Chapter 18

The Endocrine
System

Lecture Presentation by
Lee Ann Frederick
University of Texas at Arlington

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 ENDOCRINE STUDY GUIDE TEMPLATE
HORMONE SOURCE TARGET EFFECTS REGULATION

FSH Anterior Ovary Estrogen, + GnRH

Follicle Pituitary Inhibin - Inhibin
stimulating gamete prod Neg feedback
hormone
Testis Inhibin,
Gamete prod
Parathyroid Parathryroid Osteoclasts Reabsorb Direct
Hormone gland (bone) bone to regulation by
increase blood
blood calcium
Low Ca stim
Kidneys Reabsorb Ca High Ca inhib
from urine

Produce
calcitrol to
asb. Ca from
gut
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 An Introduction to the Endocrine System
• Endocrine and nervous systems regulate
homeostasis by controlling other the activities of
other organ systems

• Endocrine system uses chemical messengers

to relay information and instructions between
cells
• Hormones are chemical messengers that are
transported in the blood to target organs with
specific receptors for hormone

• Response slower but longer lasting than nervous

system
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 Endocrine System: Overview

• Controls and integrates

• Reproduction
• Growth and development
• Maintenance of electrolyte, water, and nutrient
balance of blood
• Regulation of cellular metabolism and energy
balance
• Mobilization of body defenses

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 Mechanisms of Hormone Action
• Hormones – what they do in target cells:
• Alter plasma membrane permeability (ion channels,
transporters)
• Stimulate or inhibit synthesis (transcription) of
enzymes & proteins (gene expression)
• Activate or deactivate enzymes, proteins, channels
• Phosphorylases & kinases = put P on
• Phosphatase & phosphodiesterase = take P off
• Induce secretory activity
• Stimulate mitosis

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Table 18-1 Mechanisms of Intercellular Communication.

Intercellular communication vital for

homeostasis : 4 mechanisms

Autocrine – factors that act on the cell that secretes them

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 Endocrine System: Overview

• Exocrine glands
• Nonhormonal substances (sweat, digestive enzymes)
• Have ducts to carry secretion to membrane surface

• Endocrine glands
• Produce hormones
• Lack ducts
• Product secreted into interstitial fluid so it can diffuse
into blood
• Hormones act on target cells that have receptors for
hormones & change their cell physiology

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 Endocrine System: Overview
• Endocrine glands: pituitary, thyroid, parathyroid,
adrenal, and pineal glands

• Hypothalamus is neuroendocrine organ =

• Master regulator of endocrine system
• Connection between nervous & endocrine systems

• Some organs have exocrine and endocrine functions

• Pancreas, gonads

• Many other tissues and organs produce hormones

• Adipose cells, thymus, and cells in walls of small
intestine, stomach, kidneys, and heart
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Figure 18-1 Organs and Tissues of the Endocrine System (Part 1 of 2).

Hypothalamus Pineal Gland

Production of ADH, OXT, Melatonin
and regulatory hormones

Parathyroid Glands
Pituitary Gland (located on the posterior surface
of the thyroid gland)
Anterior lobe
ACTH, TSH, GH, PRL, Parathyroid hormone (PTH)
FSH, LH, and MSH

Posterior lobe
Release of oxytocin (OXT)
and antidiuretic hormone (ADH)

Anterior lobe: regulatory hormones + prolactin & growth hormone

Posterior lobe: stores ADH & oxytocin

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Figure 18-1 Organs and Tissues of the Endocrine System (Part 2 of 2).

Organs with Secondary

Endocrine Functions

Heart See
• Atrial natriuretic peptide (ANP) Chapter
Thyroid Gland • Brain natriuretic peptide (BNP) 21
Thyroxine (T4)
Triiodothyronine (T3)
Thymus (Undergoes atrophy See
Calcitonin (CT)
during adulthood) Chapter
• Thymosins
22
Adrenal Gland
Adipose Tissue
Medulla • Leptin
Epinephrine (E)
Norepinephrine (NE)
Digestive Tract See
Cortex Secretes numerous hormones Chapter
Cortisol, corticosterone, involved in the coordination of 25
aldosterone, androgens system functions, glucose
metabolism, and appetite

Pancreatic Islets Kidneys See

• Erythropoietin (EPO) Chapters
Insulin, glucagon • Calcitriol 19 and 26

Gonads See
KEY TO PITUITARY HORMONES Testes (male) Chapters
ACTH Adrenocorticotropic hormone Androgens (especially testosterone), 28 and 29
TSH Thyroid-stimulating hormone Testis inhibin
GH Growth hormone
PRL Prolactin
FSH Follicle-stimulating hormone Ovaries (female)
LH Luteinizing hormone Ovary
Estrogens, progesterone, inhibin
MSH Melanocyte-stimulating hormone

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 Hormone Classes

Short lived
Often paracrine

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A Structural Classification of Hormones
 Chemistry of Hormones IN GENERAL
• Peptides & Proteins
• Large molecules that are water-soluble
• Their size and solubility prevent them from entering
the cell – need receptors on cell membrane,
• act by second messangers (G-protein)
• Examples are insulin and growth hormone
• Steroids
• Synthesized from cholesterol, lipid soluble
• Able to enter the cell by passing thru the cell
membrane
• Intracellular -- often nuclear
• receptor-hormone complex can bind to DNA
directly to change gene expression
• Examples are gonadal and adrenocortical
hormones
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18-1 Homeostasis and Intercellular Communication

• Target Cells
• Are specific cells that possess receptors needed
to bind and “read” hormonal messages
• ACTH receptors found only on certain cells of
adrenal cortex
• Thyroxin receptors are found on nearly all cells of
body
• On plasma membrane or intracellular
• Different cells have different combinations of
receptors so a hormone’s effect can be different in
different cells

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 Target Cell Activation

• Blood levels of hormone

• Some hormones are bound to transporters in blood
• Steroids & thryroid hormones bind to transport proteins
& albumin
• Some hormones circulate freely in blood
• Proteins & glycoproteins
• Frequency & size of pulses of released hormone
• Rate of degradation / excretion

• Relative number of receptors on or in target cell

• Affinity of binding between receptor and hormone

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 Hormones in the Blood
• Available hormone depend on amount secreted
and its removal

• Hormones removed from blood by

• Degrading enzymes in plasma & liver
• Kidneys – excretion

• Half-life—time required for hormone's blood level

to decrease by half
• Varies from fraction of minute to a week

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 18-2 Hormones

• Down-regulation
• Presence of a hormone triggers decrease in
number of hormone receptors
• When levels of particular hormone are high, cells
become less sensitive to it
• Up-regulation
• Absence of a hormone triggers increase in
number of hormone receptors
• When levels of particular hormone are low, cells
become more sensitive to it

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 18-2 Hormones

• Hormones and Plasma Membrane Receptors

• First Messengers
• Bind to receptors in plasma membrane
• Cannot have direct effect on activities inside target
cell
• Use intracellular intermediary to exert effects

• Activate second messenger on inside of plasma

membrane – this is what sends the signal
throughout the cell

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 18-2 Hormones

• G Protein
• Enzyme complex coupled to membrane receptor
• Involved in link between first messenger
(hormone) and second messenger
• G Proteins and cAMP
• G protein activates the enzyme adenylate cyclase
and changes concentration of second
messenger cyclic-AMP (cAMP) within cell

• Increased cAMP level changes metabolic activity

within cell

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Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones.
Slide 1

Recall from Chapter 3 that

G protein signaling mechanisms
are like a molecular relay race.
Hormone Receptor G protein Enzyme 2nd
1 Hormone (1st messenger) binds (1st messenger) messenger
receptor.

Adenylate cyclase Extracellular fluid

G protein (Gs)

cAMP 5 cAMP activates

GTP protein kinases.
Receptor GTP
ATP
Inactive Active
GDP GTP
protein protein
kinase kinase
Triggers responses of
target cell (activates
enzymes, stimulates
cellular secretion,
opens ion channel, etc.)

Cytoplasm

2 Receptor
activates G
3 G protein
activates
4 Adenylate
cyclase converts
G Proteins are connectors
protein (Gs). adenylate
cyclase.
ATP to cAMP (2nd
messenger).
between membrane
receptors and second
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messenger systems
Plasma Membrane Receptors and Second-
messenger Systems

• cAMP signaling mechanism:

1. Hormone (first messenger) binds to receptor
2. Receptor activates G protein
3. G protein activates adenylate cyclase
4. Adenylate cyclase converts ATP to cAMP
(second messenger)
5. cAMP activates protein kinases that
phosphorylate proteins

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Plasma Membrane Receptors and Second-
messenger Systems

• cAMP signaling mechanism

• Activated kinases phosphorylate various proteins,
activating some and inactivating others

• Intracellular enzymatic cascades have huge

amplification effect on target cell

• cAMP is rapidly degraded by enzyme

phosphodiesterase

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 A&P Flix Animation: Mechanism of Hormone
Action: Second Messenger cAMP

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Figure 18-3 G Proteins and Second Messengers (Part 1 of 2).

The first messenger A G protein is an

(a peptide hormone, enzyme complex
catecholamine, or coupled to a
eicosanoid) binds to a membrane receptor
membrane receptor and that serves as a link
activates a G protein. between the first and
second messenger.

Hormone

G proteins have 3 major Protein

Hormone

Protein
receptor receptor

ways that they send second G protein

(inactive)
G protein
activated

messengers
Effects on cAMP Levels
Many G proteins, once activated, exert their effects by changing the
concentration of cyclic AMP, which acts as the second messenger within
the cell.
Hormone Hormone

Protein Protein
receptor receptor

G protein Increased G protein Enhanced

activated production activated breakdown
of cAMP of cAMP
Acts as adenylate PDE
second cAMP cyclase ATP cAMP AMP
messenger
kinase

Reduced
Opens ion Activates enzyme
channels enzymes activity

If levels of cAMP increase, In some instances, G protein

enzymes may be activated or activation results in decreased
ion channels may be opened, levels of cAMP in the
accelerating the metabolic cytoplasm. This decrease has
activity of the cell. an inhibitory effect on the cell.

First Messenger Examples First Messenger Examples

• Epinephrine and norepinephrine • Epinephrine and norepineph-
(β receptors) rine (α2 receptors)
• Calcitonin
• Parathyroid hormone
• ADH, ACTH, FSH, LH, TSH

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 18-2 Hormones

• G Proteins and Calcium Ions

• Activated G proteins trigger:
• Opening of calcium ion channels in membrane
• Release of calcium ions from intracellular stores
• G protein activates enzyme phospholipase C (PLC)
• Enzyme triggers receptor cascade
• Production of diacylglycerol (DAG) and inositol triphosphate
(IP3) from membrane phospholipids
• DAG + calcium activates protein kinase C (PKC) which
opens channels in the plasma membrane to let extracellular
calcium into the cell
• Calcium ions may activate calmodulin, which causes further
cellular changes and amplify cell response
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Figure 18-3 G Proteins and Second Messengers (Part 2 of 2).

The first messenger A G protein is an

(a peptide hormone,
catecholamine, or
eicosanoid) binds to a
membrane receptor and
activates a G protein.
enzyme complex
coupled to a
membrane receptor
that serves as a link
between the first and
second messenger.

Hormone

Hormone

Protein Protein
receptor receptor

G protein G protein
(inactive) activated

Effects on Ca2+ Levels

Some G proteins use Ca2+ as a
second messenger.
Ca2+
Hormone

Protein
receptor

G protein
activated PLC, Opening of
DAG,
and IP3
Ca2+ channels
Release of
stored Ca2+ Ca2+ Ca2+
from ER or SER

Ca2+ acts as
second messenger Ca2+

Calmodulin

Activates
enzymes

First Messenger Examples

• Epinephrine and norepinephrine
(α1 receptors)
• Oxytocin
• Regulatory hormones of hypothalamus
• Several eicosaoids

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 Other Signaling Mechanisms

• Cyclic guanosine monophosphate (cGMP) is

second messenger for some hormones
• Some work without second messengers
• E.g., insulin receptor is tyrosine kinase enzyme
that autophosphorylates upon insulin binding 
docking for relay proteins that trigger cell
responses

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Intracellular Receptors and Direct Gene
Activation
• Steroid hormones and thyroid hormone
1. Steroids diffuse into target cells, thyroid
hormone has a transport mechanism and bind
with intracellular receptors
2. Receptor-hormone complex enters nucleus;
binds to specific region of DNA
3. Prompts DNA transcription to produce mRNA
4. mRNA directs protein synthesis (translation)
5. Promote metabolic activities, or promote
synthesis of structural proteins or proteins for
export from cell

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Figure 18-4a Effects of Intracellular Hormone Binding.
a Steroid hormones diffuse through the plasma membrane and
bind to receptors in the cytoplasm or nucleus. The complex
then binds to DNA in the nucleus, activating specific genes.

1
Diffusion through
membrane lipids

Target cell response

Testosterone stimulates CYTOPLASM

production of structural Alteration of cellular

structure or activity

proteins in skeletal muscles

6
Translation and
protein synthesis

Calcitrol (vit D) stimulates 2

Receptor

Binding of hormone
production of calcium to cytoplasmic or
nuclear receptors

transport proteins
5
Transcription and
mRNA production

Receptor 4
Gene activation
Nuclear
pore
3
Nuclear Binding of
envelope hormone–receptor
complex to DNA
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 Figure 18-4b Effects of Intracellular Hormone Binding. b Thyroid hormones enter the cytoplasm and bind to receptors in
the nucleus to activate specific genes. They also bind to
receptors on mitochondria and accelerate ATP production.

1
Transport across
plasma membrane
Target cell response

Thyroxine has receptors in Increased Alteration of cellular

ATP structure or activity
production
the nucleus and mitochondria
Receptor
6
Translation and
protein synthesis
Thyroxine stimulates 2
Binding of receptors

production of ATP by at mitochondria and

nucleus

mitochondria
5
Transcription and
mRNA production

Receptor

4
Gene activation

3
Binding of
hormone–receptor
complex to DNA
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 18-2 Hormones
• Endocrine Reflexes
• Simple Endocrine Reflex
• Involves only one hormone
• pancreas, parathyroid gland
• Complex Endocrine Reflex
• One or more intermediary steps
• Two or more hormones
• Hypothalamus → pituitary → gonads
• The hypothalamus provides highest level of
endocrine control- Master Gland

• Blood levels of hormones

• Controlled by negative feedback systems
• Vary only within narrow, desirable range
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 Figure 16.4a Three types of endocrine gland stimuli.

Humoral Stimulus
Hormone release caused by altered
levels of certain critical ions or
nutrients.

Endocrine gland stimulated to Capillary (low Ca2+

in blood)
synthesize and release
Thyroid gland
hormones in response to 3 Parathyroid
(posterior view)

types of control glands

Humoral stimuli
(calcium, glucose)
Parathyroid
glands
PTH

Stimulus: Low concentration of Ca2+ in

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capillary blood.
Response: Parathyroid glands secrete
parathyroid hormone (PTH), which
increases blood Ca2+.
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 Neural Stimulus
Hormone release caused
by neural input.
CNS (spinal cord)

Neural Stimuli = neuroendocrine

Nerve fibers stimulate hormone

release Preganglionic
Sympathetic nervous system sympathetic
fibers
fibers stimulate adrenal
medulla to secrete Medulla of
catecholamines adrenal gland

(epinephrine, also called Capillary

adrenalin)
Stimulus: Action potentials in preganglionic
Also oxytocin sympathetic fibers to adrenal medulla.
Response: Adrenal medulla cells secrete
epinephrine and norepinephrine.
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 Hormonal Stimuli
• Hormones stimulate other endocrine organs to
release their hormones
• Hypothalamic hormones stimulate release of most
anterior pituitary hormones
• Anterior pituitary hormones stimulate targets to
secrete still more hormones
• Hypothalamic-pituitary-target endocrine organ
feedback loop: hormones from final target organs
inhibit release of anterior pituitary hormones
• Glands under hypothalamic/pituitary control
• Thyroid
• Adrenal cortex
• Gonads
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 Figure 16.4c Three types of endocrine gland stimuli. Slide 1
Hormonal Stimulus
1 Brain or Hormone release caused by another
hypothalamus hormone (a tropic hormone).
Hypothalamus
gets a signal 2 Hypothalamus
that a hormone releases a
(eg testosterone RELEASING
level is low) HORMONE
Anterior
pituitary
gland
(gonadotropin
releasing
3 Anterior hormone GnRH)
Thyroid Adrenal Gonad
pituitary gland cortex (Testis)
releases
luteinizing
4 Testis
hormone (LH)
releases
testosterone
Stimulus: Hormones from hypothalamus.
Response: Anterior pituitary gland secretes
hormones that stimulate other endocrine
glands to secrete hormones.
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 Nervous System Modulation

• Nervous system modifies stimulation of endocrine

glands and their negative feedback mechanisms
• Example: under severe stress, hypothalamus and
sympathetic nervous system activated
•  body glucose levels rise

• Nervous system can override normal endocrine

controls

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Figure 18-5 Three Mechanisms of Hypothalamic Control over Endocrine Function.

Endocrine functions of the hypothalamus

1 2 3
Production of Secretion of regulatory Control of
antidiuretic hormones to control sympathetic
hormone (ADH) and activity of the anterior output to adrenal
oxytocin (OXT) lobe of pituitary gland medullae

HYPOTHALAMUS

Preganglionic
motor fibers

Infundibulum Adrenal cortex

Adrenal medulla

Posterior lobe
Anterior lobe of pituitary gland Adrenal
of pituitary gland gland

Hormones secreted by the anterior Release of antidiuretic hormone Secretion of epinephrine (E)
pituitary
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 18-10 Hormone Interactions
• Hormones Interact to Produce Coordinated
Physiological Responses
• When a cell receives instructions from two
hormones at the same time, four outcomes are
possible
1. Antagonistic effects – opposing (insulin /
glucagon)
2. Synergistic effects – additive (growth hormone
+ glucocorticoids)
3. Permissive effects – one hormone is necessary
for another to produce effect (norepinephrine
/thyroid hormone
4. Integrative effects – hormones produce
different and complementary results (PTH
/Calcitrol)
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 The Pituitary Gland and Hypothalamus

• Pituitary is connected to hypothalamus by

infundibulum

• Pituitary gland (hypophysis) has two

major lobes
• Posterior pituitary (neurohypohpysis)
• Neural tissue
• Anterior pituitary (adenohypophysis)
• Glandular tissue

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Figure 18-6a The Anatomy and Orientation of the Pituitary Gland.

Third Mammillary
ventricle body

Hypothalamus

Optic chiasm
Infundibulum
Sellar diaphragm

Anterior pituitary lobe

Pars tuberalis
Pars distalis Posterior
pituitary
Pars intermedia lobe

Sphenoid
(sella turcica)

a Relationship of the pituitary

gland to the hypothalamus
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Figure 18-6b The Anatomy and Orientation of the Pituitary Gland.

Anterior pituitary lobe Posterior

pituitary
Pars Pars lobe
distalis intermedia

Secretes other Secretes Releases

pituitary hormones MSH ADH and OXT

Pituitary gland LM × 77

b Histology of the pituitary gland showing the

anterior and posterior lobes
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Figure 18-7 The Hypophyseal Portal System and the Blood Supply to the Pituitary Gland.

Supraoptic nuclei Paraventricular nuclei Neurosecretory neurons

Mammillary
body

Optic The superior hypophyseal artery delivers blood

chiasm to the capillary network in the median
eminence

Capillary network in
the median eminence
The portal vessels deliver blood containing
Infundibulum regulatory factors to the capillary network
within the anterior lobe of the pituitary gland
Anterior lobe of
the pituitary gland
Capillary network in The inferior hypophyseal artery delivers blood
the anterior lobe to the posterior lobe of the pituitary gland
Posterior lobe of
the pituitary gland

Endocrine cells Hypophyseal veins carry blood containing the

pituitary hormones to the cardiovascular
system for delivery to the rest of the body

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 Pituitary-hypothalamic Relationships

• Posterior pituitary (lobe)

• Downgrowth of hypothalamic neural tissue
• Neural connection to hypothalamus
(hypothalamic-hypophyseal tract)

• Nuclei of hypothalamus synthesize

neurohormones oxytocin and antidiuretic
hormone (ADH)

• Neurohormones are transported to and stored

in posterior pituitary

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 The hypothalamus controls release of hormones from the
pituitary gland in two different ways.

Paraventricular nucleus

Hypothalamus 1 Hypothalamic neurons

synthesize oxytocin or
antidiuretic hormone (ADH).
Posterior lobe
of pituitary
Optic
chiasma
Supraoptic
nucleus
Infundibulum 2 Oxytocin and ADH are
(connecting stalk)
transported down the axons of the
Inferior hypothalamic- hypophyseal tract to
Hypothalamic- hypophyseal the posterior pituitary.
hypophyseal artery
tract
Axon terminals
3 Oxytocin and ADH are
stored in axon terminals in the
Posterior lobe posterior pituitary.
of pituitary
Oxytocin 4
When hypothalamic neurons fire,
ADH action potentials arriving at the
axon terminals cause oxytocin or
ADH to be released into the blood.
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 Pituitary-hypothalamic Relationships

• Anterior Lobe (adenohypothesis):

• Originates as out-pocketing of oral mucosa
• Vascular connection to hypothalamus
• Hypophyseal portal system consists of:
• Primary capillary plexus
• Hypophyseal portal veins
• Secondary capillary plexus
• Carries releasing and inhibiting hormones to
anterior pituitary to regulate hormone secretion
-- it regulates many endocrine glands

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 The hypothalamus controls release of hormones from the
pituitary gland in two different ways.

Hypothalamus Hypothalamic
neurons synthesize
GHRH, GHIH, TRH,
Anterior lobe CRH, GnRH, PIH.
of pituitary Superior
hypophyseal
artery 1 When appropriately stimulated,
2 Hypothalamic hormones travel hypothalamic neurons secrete
through portal veins to the anterior releasing or inhibiting hormones into
pituitary where the primary capillary plexus.
they stimulate or inhibit Hypophyseal
release of hormones made in the
anterior pituitary. portal system
• Primary capillary
3 In response to releasing plexus A portal
hormones, the anterior pituitary • Hypophyseal system is
secretes hormones into the two
secondary capillary plexus. This portal veins capillary
in turn empties into the general • Secondary plexuses
circulation. capillary plexus (beds)
connected
GH, TSH, ACTH, by veins.
FSH, LH, PRL
Anterior lobe
of pituitary

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Posterior Pituitary and Hypothalamic Hormones

• Oxytocin and ADH

• Each composed of nine amino acids
• Almost identical – differ in two amino acids
• Synthesized in hypothalamus
• No hypothalamic releasing or inhibiting hormones
to regulate secretion
• Stored in posterior lobe of pituitary
• RELEASE
• ADH = osmoreceptors in hypothalamus
• Oxytocin = sensory neurons, uterus/breast

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Figure 18-9 Pituitary Hormones and Their Targets (Part 2 of 2).

Hypothalamus KEY TO PITUITARY HORMONES:

Direct Release ACTH Adrenocorticotropic hormone
of Hormones TSH Thyroid-stimulating hormone
Sensory Osmoreceptor GH Growth hormone
stimulation stimulation PRL Prolactin
FSH Follicle-stimulating hormone
LH Luteinizing hormone
MSH Melanocyte-stimulating hormone
ADH Antidiuretic hormone
OXT Oxytocin

Posterior lobe
of pituitary gland

ADH

Kidneys
OXT
Males: Smooth
muscle in ductus
deferens and
prostate gland

Females: Uterine
smooth muscle and
mammary glands
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 Oxytocin

• Strong stimulant of uterine contraction

• Released during childbirth
• Hormonal trigger for milk ejection
• Nuzzle nipple stimulate milk let down
• Hear baby cry stimulate milk let down (neural)
• Stress & anxiety can inhibit milk let down (neural)
• Acts as neurotransmitter in brain

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 ADH (Antidiruetic Hormone / Vasopressin)

• Inhibits or prevents urine formation

• Regulates water balance
• Targets kidney tubules  reabsorb more
water
• Release also triggered by pain, low blood
pressure, and drugs
• Inhibited by alcohol, diuretics
• High concentrations  vasoconstriction

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 ADH

• Diabetes insipidus
• ADH deficiency due to hypothalamus or posterior
pituitary damage
• Must keep well-hydrated

• Syndrome of inappropriate ADH secretion

(SIADH)
• Retention of fluid, headache, disorientation
• Fluid restriction; blood sodium level monitoring

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 Anterior Pituitary Hormone – all are proteins

• Growth hormone (GH) –direct + tropic hormone

Control
• Thyroid-stimulating hormone (TSH) or the
thyrotropin release of
• Adrenocorticotropic hormone (ACTH) other
hormones
• Follicle-stimulating hormone (FSH) = TROPIC
• Luteinizing hormone (LH) hormones

• Prolactin (PRL) – direct hormone

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 Anterior pituitary is controlled by the
hypothalamus PLUS negative feed back from
hormones is causes to be secreted
• Hypothalamic Control of the Anterior Lobe
• Two classes of hypothalamic regulatory hormones
1. Releasing hormones (RH) -- most
• Stimulate synthesis and secretion of one or more hormones
at anterior lobe
2. Inhibiting hormones (IH) -prolatctin, GH
(somatostatin)
• Prevent synthesis and secretion of hormones from the
anterior lobe

• Rate of synthesis & secretion is controlled by

negative feedback
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Figure 18-8a Feedback Control of Endocrine Secretion.

Feedback Control of Endocrine

Secretion at the Hypothalamus
Typical Pattern of Regulation when
Multiple Endocrine Organs Are Involved

Hypothalamus

RH

Pituitary
gland

Anterior
lobe

Hormone 1 Negative
feedback

Endocrine
organ

Hormone 2

KEY
Target cells Stimulation
Inhibition

a The hypothalamus produces a releasing

hormone (RH) to stimulate hormone
production by other glands. Control
occurs by negative feedback.

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 Feedback Control of Endocrine
Secretion at the Hypothalamus
Variations on the Typical Pattern of Regulation
of Endocrine Organs by the Hypothalamus
and Anterior Pituitary Lobe
Feedback Control of Endocrine
Secretion at the Hypothalamus
Variations on the Typical Pattern of Regulation
of Endocrine Organs by the Hypothalamus
and Anterior Pituitary Lobe

Stimulation Stimulation
GH–IH PIH
GH–RH
Inhibition Inhibition
PRF

Anterior
lobe Anterior
lobe
Epithelia,
GH adipose tissue,
liver
PRL
Liver

Somatomedins Stimulates
mammary
glands
Stimulates growth of
skeletal muscle, cartilage,
and many other tissues

b The regulation of prolactin (PRL) production

c The regulation of growth hormone by the anterior lobe. In this case, the
(GH) production by the anterior lobe. hypothalamus produces both a releasing
When GH–RH release is inhibited, factor (PRF) and an inhibiting hormone (PIH).
GH–IH release is stimulated. When one is stimulated, the other is inhibited.

© 2015 Pearson Education, Inc.

Figure 18-8d Feedback Control of Endocrine Secretion.
Target Effects on
hormone body +
Hypothalamus Pituitary synthesis negative
& release feedback
Releasing Hormone 1 Endocrine Hormone 2
hormone (RH) (from pituitary) target organ (from target organ)

TRH TSH Thyroid gland Thyroid hormones

CRH ACTH Adrenal cortex Glucocorticoids

Testes Inhibin
FSH Inhibin
Ovaries
Estrogens
GnRH
Testes Androgens
LH Progesterone
Ovaries
Estrogens

d Table showing the hypothalamic releasing hormones that follow

the typical pattern of regulation shown in a above.
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© 2013 Pearson Education, Inc.

Growth Hormone (GH, or Somatotropin)

GH-RH // GH-IH (somatostatins)
• Direct actions on metabolism: epithelial cells,
connective tissue, adipose, liver
• Epithelia & connective tissue: cell division &
differentiation
• Adipose tissue: breakdown of triglycerides to
fatty acids = glucose sparing effect
• Liver : breakdown of glycogen (diabetogenic
effects) & synthesis of somatomedins (IGF’s)

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© 2013 Pearson Education, Inc.

Growth Hormone
(GH, or Somatotropin)

• Indirect actions on growth

• Mediates growth via growth-promoting proteins –
insulin-like growth factors (IGFs) and
somatomedins synthesized by the liver
• IGFs stimulate
• Uptake of nutrients used for synthesis of DNA and
proteins – especially amino acids
• Formation of collagen and deposition of bone
matrix
• Major targets—bone and skeletal muscle

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© 2013 Pearson Education, Inc.

Growth-promoting and metabolicHypothalamus

actions of growth hormone
secretes growth
Feedback Inhibits GHRH release
hormone–releasing
Stimulates GHIH release hormone (GHRH), and
Anterior
pituitary GHIH (somatostatin)
Inhibits GH synthesis
and release

Growth hormone (GH)

Indirect actions Direct actions

(growth- (metabolic,
promoting) anti-insulin)

Liver and
other tissues

Produce

Insulin-like growth
factors (IGFs)

Effects Effects

Fat Carbohydrate
Skeletal Extraskeletal
metabolism metabolism

Increases, stimulates
Reduces, inhibits
Increased protein Initial stimulus
Increased cartilage Increased Increased blood
synthesis, and
formation and fat breakdown glucose and other Physiological response
cell growth and
skeletal growth and release anti-insulin effects
proliferation Result

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© 2013 Pearson Education, Inc.

Homeostatic Imbalances of Growth Hormone

• Hypersecretion
• In children results in
gigantism
• In adults results in
acromegaly
• Hyposecretion
• In children results in
pituitary dwarfism

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© 2013 Pearson Education, Inc.

Prolactin (PRL)

• Regulation of PRL release

• Primarily controlled by prolactin-inhibiting
hormone (PIH) (dopamine)
• Blood levels rise toward end of pregnancy
• Suckling stimulates PRL release and promotes
continued milk production
• Milk production is dependent on the interactions
of several hormones including prolactin, estrogen,
progesterone, glucocorticoids + placental
hormones

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© 2013 Pearson Education, Inc.

Figure 16.8 Regulation of thyroid hormone secretion.

Hypothalamus

TRH

Anterior pituitary

TSH
Synthesis and
Thyroid gland release of thyroid
hormones T3/T4
Thyroid
hormones
Stimulates
Target cells
Inhibits
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© 2013 Pearson Education, Inc.

Adrenocorticotropic Hormone (ACTH /

Corticotropin)

• Stimulates adrenal cortex to release corticosteroids

(glucocorticoids)

• Regulation of ACTH release

• Triggered by hypothalamic corticotropin-releasing
hormone (CRH) in daily rhythm (circadian rhythm)
• Rises as approach active part of day, decreases as
approach resting part of day (ie night)

• Rises with stress

• Internal and external factors such as fever, hypoglycemia,
and stressors can alter release of CRH
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© 2013 Pearson Education, Inc.

Gonadotropins
• Follicle-stimulating hormone (FSH) and luteinizing
hormone (LH)

• FSH stimulates gamete (ova (egg) or sperm)

production + production of inhibin

• LH promotes production of gonadal hormones

(males: testosterone, females: estrogen &
progesterone)

• Absent from the blood in prepubertal boys and girls

• Elevated in postmenopausal women
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© 2013 Pearson Education, Inc.

Gonadotropins
• Regulation of gonadotropin release
• Triggered by gonadotropin-releasing hormone
(GnRH) during and after puberty

• Suppressed by gonadal hormones (neg feedback)

• FSH: inhibin
• LH: sex steroids
• Positive feedback during ovulatioin in females

• Birth control takes advantage of negative

feedback to prevent maturation and ovulation of a
women’s ova (eggs)

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Figure 18-9 Pituitary Hormones and Their Targets (Part 1 of 2).

Hypothalamus KEY TO PITUITARY HORMONES:

Direct Control Indirect Control through Release ACTH Adrenocorticotropic hormone
by Nervous of Regulatory Hormones TSH Thyroid-stimulating hormone
System GH Growth hormone
Regulatory hormones are released
into the hypophyseal portal system PRL Prolactin
for delivery to the anterior lobe of FSH Follicle-stimulating hormone
the pituitary gland LH Luteinizing hormone
MSH Melanocyte-stimulating hormone
ADH Antidiuretic hormone
OXT Oxytocin

Anterior lobe of
Adrenal pituitary gland
medulla
ACTH
Pituitary Summary 1
Adrenal
gland
Adrenal
TSH GH
cortex

Epinephrine and Liver MSH

Thyroid
norepinephrine PRL FSH LH
gland
Somatomedins

IGF
Glucocorticoids
(cortisol, Melanocytes (uncertain
corticosterone) significance in healthy
adults)
Bone, muscle, Ovaries
Testes of female
other tissues Mammary
of male
glands
Thyroid
hormones (T3, T4)
Inhibin Testosterone Estrogen Progesterone Inhibin
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Table 18-2 The Pituitary Hormones (Part 1 of 2).

Pituitary Summary 2
© 2015 Pearson Education, Inc.
Figure 18-9 Pituitary Hormones and Their Targets (Part 2 of 2).

Hypothalamus KEY TO PITUITARY HORMONES:

Direct Release ACTH Adrenocorticotropic hormone
of Hormones TSH Thyroid-stimulating hormone
Sensory Osmoreceptor GH Growth hormone
stimulation stimulation PRL Prolactin
FSH Follicle-stimulating hormone
LH Luteinizing hormone
MSH Melanocyte-stimulating hormone
ADH Antidiuretic hormone
OXT Oxytocin

Posterior lobe
of pituitary gland

ADH

Kidneys
OXT
Males: Smooth
muscle in ductus
deferens and
prostate gland

Females: Uterine
smooth muscle and
Pituitary Summary 3 mammary glands
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Table 18-2 The Pituitary Hormones (Part 2 of 2).

Pituitary Summary 4
© 2015 Pearson Education, Inc.
 18-4 The Thyroid Gland

• The Thyroid Gland

• Lies inferior to thyroid cartilage of larynx
• Consists of two lobes connected by narrow
isthmus
• Thyroid follicles
• Hollow spheres lined by cuboidal epithelium
• Cells surround follicle cavity that contains viscous
colloid
• Surrounded by network of capillaries that:
• Deliver nutrients and regulatory hormones
• Accept secretory products and metabolic wastes

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Figure 18-10a The Thyroid Gland.

Hyoid bone

Superior
thyroid artery

Thyroid cartilage
of larynx Internal
jugular vein
Superior
thyroid vein
Cricoid cartilage
Common of larynx
carotid artery Left lobe of
Right lobe of thyroid gland
thyroid gland
Isthmus of
Middle thyroid vein thyroid gland

Inferior
thyroid artery
Thyrocervical trunk
Inferior
thyroid
Trachea veins

Outline of clavicle

Outline of sternum

a Location and anatomy of the thyroid gland

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Figure 18-10c The Thyroid Gland.

Capillary
Capsule C cell

Cuboidal
epithelium
Follicle of follicle
cavities
Thyroid
follicle
Thyroid Thyroglobulin
follicle stored in colloid
of follicle

C cell

Follicles of the thyroid gland LM × 260

c Histological details of the thyroid gland showing thyroid follicles and both cell
types in the follicular epithelium ATLAS: Plate 18c

Thyroid stores thryroglobulin in the follicle

lumens – like having a giant pantry just for
thyroxine
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 18-4 The Thyroid Gland
• Thyroglobulin (Globular Protein)
• Synthesized by follicle cells
• Secreted into colloid of thyroid follicles
• Molecules contain the amino acid tyrosine
• Thyroxine (T4) – most abundant
• Also called tetraiodothyronine
• Contains four iodide ions
• Triiodothyronine (T3) – most active
• Contains three iodide ions
• Effects virtually every cell in the body
• In children, essential to normal development of:
• Skeletal, muscular, and nervous systems
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 Synthesis of Thyroid Hormone
• Thyroid gland stores hormone extracellularly
– only hormone stored extracellularly and in
such large quantities

• TSH required for synthesis and secretion of

T3/T4

© 2015 Pearson Education, Inc.

Figure 16.10 Synthesis of thyroid hormone.
Slide 2
Thyroid follicular cells

Colloid

1 Thyroglobulin is synthesized and

discharged into the follicle lumen. Tyrosines (part of thyroglobulin
molecule)
Capillary

Golgi
apparatus

Rough
ER

Colloid in
lumen of
follicle

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Pearson Education,
Education, Inc.
Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 3
Thyroid follicular cells

Colloid

1 Thyroglobulin is synthesized and

discharged into the follicle lumen. Tyrosines (part of thyroglobulin
molecule)
Capillary

Golgi
apparatus

Rough
ER

Iodide (I−) 2 Iodide (I–) is trapped

(actively transported in).

Colloid in
lumen of
follicle

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Pearson Education,
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Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 4
Thyroid follicular cells

Colloid

1 Thyroglobulin is synthesized and

discharged into the follicle lumen. Tyrosines (part of thyroglobulin
molecule)
Capillary

Golgi
apparatus

Rough
ER Iodine
3 Iodide
is oxidized
to iodine.

Iodide (I−) 2 Iodide (I–) is trapped

(actively transported in).

Colloid in
lumen of
follicle

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Pearson Education,
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Figure 16.10 Synthesis of thyroid hormone.
Slide 5
Thyroid follicular cells

Colloid

1 Thyroglobulin is synthesized and

discharged into the follicle lumen. Tyrosines (part of thyroglobulin
molecule)
Capillary
4 Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Golgi
apparatus

Rough Thyro-
ER Iodine
globulin
3 Iodide DIT MIT
colloid
is oxidized
to iodine.

Iodide (I−) 2 Iodide (I–) is trapped

(actively transported in).

Colloid in
lumen of
follicle

Iodine attaches to tyrosine,

mediated by peroxidase enzymes
© 2015 Pearson Education, Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 6
Thyroid follicular cells

Colloid

1 Thyroglobulin is synthesized and

discharged into the follicle lumen. Tyrosines (part of thyroglobulin
molecule)
Capillary
4 Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Golgi
apparatus

Rough Thyro-
ER Iodine
globulin
3 Iodide DIT MIT
colloid
is oxidized
to iodine.

Iodide (I−) 2 Iodide (I–) is trapped

(actively transported in). T4 5 Iodinated tyrosines are
T3 linked together to form T3
and T4.

Colloid in
lumen of
follicle

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Figure 16.10 Synthesis of thyroid hormone.
Slide 7
Thyroid follicular cells

Colloid

1 Thyroglobulin is synthesized and

discharged into the follicle lumen. Tyrosines (part of thyroglobulin
molecule)
Capillary
4 Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Golgi
apparatus

Rough Thyro-
ER Iodine
globulin
3 Iodide DIT MIT
colloid
is oxidized
to iodine.

Iodide (I−) 2 Iodide (I–) is trapped

(actively transported in). T4 5 Iodinated tyrosines are
T3 linked together to form T3
Lysosome and T4.

6 Thyroglobulin colloid is
endocytosed and combined
with a lysosome.
Colloid in
lumen of
follicle

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Pearson Education,
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Figure 16.10 Synthesis of thyroid hormone.
Slide 8
Thyroid follicular cells

Colloid

1 Thyroglobulin is synthesized and

discharged into the follicle lumen. Tyrosines (part of thyroglobulin
molecule)
Capillary
4 Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Golgi
apparatus

Rough Thyro-
ER Iodine
globulin
3 Iodide DIT MIT
colloid
is oxidized
to iodine.

Iodide (I−) 2 Iodide (I–) is trapped

(actively transported in). T4 5 Iodinated tyrosines are
T3 linked together to form T3
Lysosome and T4.

T4
6 Thyroglobulin colloid is
endocytosed and combined
T3
7 Lysosomal enzymes with a lysosome.
T4 Colloid in
cleave T4 and T3 from
lumen of
T3 thyroglobulin and hormones
diffuse into bloodstream. follicle

To peripheral tissues

© 2015 Pearson Education, Inc.

Figure 16.10 Synthesis of thyroid hormone.
Slide 1
Thyroid follicular cells

Colloid

1 Thyroglobulin is synthesized and

discharged into the follicle lumen. Tyrosines (part of thyroglobulin
molecule)
Capillary
4 Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Golgi
apparatus

Rough Thyro-
ER Iodine
globulin
3 Iodide DIT MIT
colloid
is oxidized
to iodine.

Iodide (I−) 2 Iodide (I–) is trapped

(actively transported in). T4 5 Iodinated tyrosines are
T3 linked together to form T3
Lysosome and T4.

T4
6 Thyroglobulin colloid is
endocytosed and combined
T3
7 Lysosomal enzymes with a lysosome.
T4 Colloid in
cleave T4 and T3 from
lumen of
T3 thyroglobulin and hormones
diffuse into bloodstream. follicle

To peripheral tissues

© 2015 Pearson Education, Inc.

Figure 18-11a The Thyroid Follicles.

Follicle
cavity

3 Thyroglobulin
FOLLICLE CAVITY
(contains T3 and T4)

4 Endocytosis

2 Thyroglobulin

Iodine 5 Lysosomal
atoms (I0) Other amino acids digestion

Tyrosine T4
T3

Diffusion

TSH- Diffusion 6
sensitive
ion pump FOLLICLE CELL
1
7
CAPILLARY

Iodide ions (I−)

TBG, transthyretin,
T4 & T3 or albumin
a The synthesis, storage, and secretion of thyroid
hormones. The numbered events are explained in the text.
© 2015 Pearson Education, Inc.
 Synthesis of Thyroid Hormone
• Thyroid gland stores hormone extracellularly
– only hormone stored extracellularly and in
such large quantities
• Thyroglobulin synthesized and discharged into
follicle lumen
• Iodides (I–) actively taken into cell and released
into lumen
• Iodide oxidized to iodine (I2),
• Iodine attaches to tyrosine, mediated by
peroxidase enzymes

© 2015 Pearson Education, Inc.

 Synthesis of Thyroid Hormone

• Iodinated tyrosines link together to form T3 and T4

• Colloid is endocytosed and combined with
lysosome
• T3 and T4 are cleaved and diffuse into
bloodstream

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Figure 18-11b The Thyroid Follicles.

Hypothalamus
releases TRH
Homeostasis
Disturbed
Decreased T3 and TRH
T4 concentrations
in blood or low
body temperature
Anterior
lobe
Pituitary
gland
HOMEOSTASIS
Normal T3 and T4 Anterior
concentrations, lobe
normal body
temperature
TSH

Homeostasis
Restored
Increased T3 and
T4 concentrations Thyroid
in blood gland

Thyroid follicles
release T3 and T4

b The regulation of thyroid secretion.

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© 2013 Pearson Education, Inc.

Transport and Regulation of TH

• Negative feedback regulation of TH release

• Rising TH levels provide negative feedback
inhibition on release of TSH

• Hypothalamic thyrotropin-releasing hormone

(TRH) can overcome negative feedback during
pregnancy or exposure to cold

© 2015 Pearson Education, Inc.

 Transport and Regulation of TH

• T4 and T3 transported by thyroxine-binding

globulins (TBGs)
• Both bind to target receptors, but T3 is ten
times more active than T4
• T3/T4 transported into the cell
• Bind to intracellular receptors
• Cytoplasm
• Nucleus
• mitochondia
• Peripheral tissues convert T4 to T3

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 18-4 The Thyroid Gland

• Effects of Thyroid Hormones on Peripheral Tissues

1. Elevates rates of oxygen consumption and energy
consumption; in children, may cause a rise in body
temperature
2. Increases heart rate and force of contraction;
generally results in a rise in blood pressure
3. Increases sensitivity to sympathetic stimulation
4. Maintains normal sensitivity of respiratory centers to
changes in oxygen and carbon dioxide concentrations
5. Stimulates red blood cell formation and thus enhances
oxygen delivery
6. Stimulates activity in other endocrine tissues–
reproductive functions
7. Accelerates turnover of minerals in bone

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 18-4 The Thyroid Gland
• Calorigenic Effect
• Cell consumes more energy resulting in increased
heat generation

• Is responsible for strong, immediate, and short-

lived increase in rate of cellular metabolism

• Increases enzymes for glycolysis and ATP

production

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© 2013 Pearson Education, Inc.

Homeostatic Imbalances of TH

• Hyposecretion in adults—myxedema; goiter if

due to lack of iodine
• In US iodine is added to table salt so goiter is now
rare
• Hyposecretion in infants—cretinism
• Brain does not develop properly
• Essential for normal skeletal & muscular
development
• Hypersecretion—Graves' disease
• Autoimmune disease to receptor for thyrotropin so
negative feed back does not occur
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 18-4 The Thyroid Gland

• The C Cells of the Thyroid Gland and Calcitonin

• C (clear) cells also called parafollicular cells
• Produce calcitonin (CT)
• Helps regulate concentrations of Ca2+ in body fluids
1. Inhibits osteoclasts, which slows the rate of Ca2+
release from bone
2. Stimulates Ca2+ excretion by the kidneys
3. Probably most important in children during
skeletal growth

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 18-5 Parathyroid Glands

• Four Parathyroid Glands

• Embedded in the posterior surface of the thyroid
gland
• Altogether, the four glands weigh 1.6 g
• Parathyroid Hormone (PTH) or parathormone
• Produced by parathyroid (chief) cells in
response to low concentrations of Ca2+
• Antagonist for calcitonin
• MOST IMPORTANT hormone for regulation of
blood calcium levels

© 2015 Pearson Education, Inc.

 Figure 18-12a The Parathyroid Glands.

Left lobe of
thyroid gland

Parathyroid
glands

a Thyroid gland, posterior view. The

location of the parathyroid glands
on the posterior surface of the
thyroid lobes. (The thyroid lobes are
located anterior to the trachea.)
© 2015 Pearson Education, Inc.
Figure 18-12b The Parathyroid Glands.

Blood vessel

Connective tissue capsule

of parathyroid gland

Thyroid
follicle
Parathyroid gland LM × 94

b Both parathyroid and

thyroid tissues.

© 2015 Pearson Education, Inc.

 18-5 Parathyroid Glands
• Three Effects of PTH- increase blood calcium
1. It stimulates osteoclasts and inhibits
osteoblasts
• Accelerates mineral turnover and releases Ca2+
from bone
• Reduces rate of calcium deposition in bone
2. It enhances reabsorption of Ca2+ at kidneys,
reducing urinary losses
3. It stimulates formation and secretion of calcitriol
by the kidneys
• Effects complement or enhance PTH
• Also enhances Ca2+, PO43 absorption by
digestive tract
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© 2013 Pearson Education, Inc.
Figure 16.13 Effects of parathyroid hormone on bone, the kidneys, and the intestine.

Hypocalcemia
(low blood Ca2+)

PTH release from

parathyroid gland

Osteoclast activity Ca2+ reabsorption Activation of

in bone causes Ca2+ in kidney tubule vitamin D by kidney
and PO43- release
into blood

Ca2+ absorption
from food in small
intestine

Ca2+ in blood

Initial stimulus
Physiological response
Result
© 2015 Pearson Education, Inc.
Figure 18-13 The Homeostatic Regulation of Calcium Ion Concentrations (Part 1 of 2).

Increased
excretion
Parathyroid of calcium
produces by kidneys

LESS PTH Thyroid gland

produces Calcium
calcitonin deposition
in bone
Increasing levels of blood calcium

HOMEOSTASIS
HOMEOSTASIS RESTORED
DISTURBED
Blood calcium
levels decrease
Increasing calcium
levels in blood

HOMEOSTASIS

Normal blood
Parathyroid
calcium levels produces
(8.5–11 mg/dL)
MORE PTH
© 2015 Pearson Education, Inc.
Figure 18-13 The Homeostatic Regulation of Calcium Ion Concentrations (Part 2 of 2).

Direct regulation
HOMEOSTASIS
by blood calcium

Decreasing levels of blood calcium

Normal blood
calcium levels levels!
(8.5–11 mg/dL)

HOMEOSTASIS
HOMEOSTASIS
DISTURBED
RESTORED

Decreasing calcium Blood calcium

levels in blood levels increase

Increased
reabsorption of
calcium by
Parathyroid kidneys
glands secrete
Calcium release
parathyroid
hormone (PTH) from bone

Increased calcitriol
production causes
Ca2+ absorption
by digestive tract
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Homeostatic Imbalances of PTH

• Hyperparathyroidism due to tumor

• Bones soften and deform
• Elevated Ca2+ depresses nervous system and
contributes to formation of kidney stones

• Hypoparathyroidism following gland trauma or

removal or dietary magnesium deficiency
• Results in tetany, respiratory paralysis, and death

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Table 18-4 Hormones of the Thyroid Gland and Parathyroid Glands.

© 2015 Pearson Education, Inc.

 18-6 Adrenal Glands

• The Adrenal Glands

• Lie along superior border of each kidney
• Subdivided into:
• Superficial adrenal cortex
• Stores lipids, especially cholesterol and fatty acids
• Manufactures steroid hormones (corticosteroids)
• Inner adrenal medulla
• Secretory activities controlled by sympathetic
division of ANS
• Produces epinephrine (adrenaline) and
norepinephrine (catecholamines)
• Metabolic changes persist for several minutes

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Figure 18-14a The Adrenal Gland.
Right superior Right and left inferior
adrenal arteries phrenic arteries
Celiac trunk

Right adrenal Left adrenal gland

gland

Right middle Left middle

adrenal artery adrenal artery
Right inferior Left inferior
adrenal artery adrenal arteries
Left adrenal vein
Right renal
artery Left renal artery
Left renal vein
Right renal vein
Superior
mesenteric artery
Abdominal aorta
Inferior vena cava
a A superficial view of the
kidneys and adrenal glands

Capsule
Cortex
Medulla
b

b An adrenal gland
in section

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 Figure 16.14 Microscopic structure of the adrenal gland.

Three layers of cortex produce the different corticosteroids.

Them medulla produces catecholamines.

Hormones
Capsule secreted
Zona Aldosterone
glomerulosa mineralcorticoid

Zona Cortisol
fasciculata Glucocorticoids
Adrenal gland
Cortex

• Medulla
• Cortex

Kidney
Zona Androgens
reticularis Male sex hormones
Medulla

Adrenal
medulla Epinephrine
and
norepinephrine

Drawing of the histology of the Photomicrograph (115x)

adrenal cortex and a portion of
© 2015 Pearson Education, Inc. the adrenal medulla
 18-6 Adrenal Glands
• Aldosterone most potent mineralocorticoid
• Stimulates conservation of sodium ions and
elimination of potassium ions
• Water follows sodium

• Secretion in response to:

• Drop in blood Na+, blood volume, or blood pressure
• Increase in K+

• Works with ADH to conserve water and raise

blood pressure

© 2015 Pearson Education, Inc.

 Figure 16.15 Major mechanisms controlling aldosterone release from the adrenal cortex.

Primary regulators Other factors

Blood volume K+ in blood Stress Blood pressure

and/or blood and/or blood
pressure volume

Hypo- Heart
thalamus
Kidney

CRH
Direct Anterior
stimulating pituitary
Renin effect

Initiates
cascade
that
produces
ACTH Atrial natriuretic
peptide (ANP)
Angiotensin II

Inhibitory
effect
Zona glomerulosa
of adrenal cortex
Enhanced
secretion
of aldosterone

Targets
kidney tubules

Absorption of Na+ and

water; increased K+ excretion

Blood volume
and/or blood pressure

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 Mechanisms of Aldosterone Secretion

• Renin-angiotensin-aldosterone mechanism:
decreased blood pressure stimulates kidneys to
release renin  triggers formation of angiotensin
II, a potent stimulator of aldosterone release
• Plasma concentration of K+: increased K+
directly influences zona glomerulosa cells to
release aldosterone
• ACTH: causes small increases of aldosterone
during stress
• Atrial natriuretic peptide (ANP, heart): blocks
renin and aldosterone secretion to decrease
blood pressure
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 Homeostatic Imbalances of Aldosterone

• Aldosteronism—hypersecretion due to adrenal

tumors
• Hypertension and edema due to excessive Na+

• Excretion of K+ leading to abnormal function of

neurons and muscle

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 18-6 Adrenal Glands

• Zona Fasciculata
• Produces glucocorticoids

• For example, cortisol (hydrocortisone) with

corticosterone
• Liver converts cortisol to cortisone

• Secretion stimulated by ACTH & negative

feedback

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 Glucocorticoids: Cortisol

• Released in response to ACTH, patterns of eating

and activity, and stress
• Prime metabolic effect is gluconeogenesis—
formation of glucose from fats and proteins
• Promotes rises in blood glucose, fatty acids, and
amino acids
• "Saves" glucose for brain
• Enhances vasoconstriction  rise in blood
pressure to quickly distribute nutrients to cells

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 Actions of Cortisol
• Primary actions involve three different targets:
• Liver
• Skeletal muscle
• Adipose tissue

• Actions of cortisol are mostly catabolic

• Help maintain proper levels of blood glucose and
other nutrients during fasting conditions

• Permissive effects of cortisol:

• Enhances lipid breakdown by epinephrine in
adipose tissue

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 Anti-inflammatory and
Immunosuppressive Effects

• Decreases the numbers of some white blood

cells
• At high concentrations act to suppress some
portions of the immune response

• At high concentrations glucocorticoids block most

steps in the inflammatory response
• Vasodilation
• Phagocytosis, etc.

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 Homeostatic Imbalances of Glucocorticoids

• Hypersecretion—Cushing's syndrome/disease
• Depresses cartilage and bone formation
• Inhibits inflammation
• Depresses immune system
• Disrupts cardiovascular, neural, and
gastrointestinal function
• Hyposecretion—Addison's disease
• Also involves deficits in mineralocorticoids
• Decrease in glucose and Na+ levels
• Weight loss, severe dehydration, and hypotension

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 18-6 Adrenal Glands
• Zona Reticularis
• Network of endocrine cells
• Forms narrow band bordering each adrenal
medulla
• Produces weak androgens under stimulation
by ACTH

• In adult women
• Muscle mass
• Blood cell formatin (erythropoiesis)
• Sex drive
• Can be converted to estrogen after menopause

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Figure 18-14c The Adrenal Gland.

The Adrenal Hormones

Region/Zone Hormones Primary Target Hormonal Effects Regulatory Control

ADRENAL CAPSULE

ADRENAL CORTEX Increase renal reabsorption Stimulated by angiotensin II,

Zona Mineralocorticoids, Kidneys of Na+ and water (especially elevated blood K+ or fall in
glomerulosa primarily in the presence of ADH), and blood Na+; inhibited by ANP
aldosterone accelerate urinary loss of K+ and BNP

Zona fasciculata Glucocorticoids Most cells Increase rates of glucose and Stimulated by ACTH
(cortisol glycogen formation by the from the anterior lobe of
[hydrocortisone], liver; release of amino acids the pituitary gland
corticosterone) from skeletal muscles, and
lipids from adipose tissues;
promote peripheral utilization
of lipids; anti-inflammatory
effects

Zona reticularis Androgens Adrenal androgens stimulate Androgen secretion is

Most cells
the development of pubic stimulated by ACTH.
hair in boys and girls before
puberty.

ADRENAL MEDULLA Epinephrine (E), Most cells Increases cardiac activity, Stimulated by sympathetic
norepinephrine blood pressure, glycogen preganglionic fibers
(NE) breakdown, blood glucose
levels; releases lipids by
Adrenal gland LM × 140
adipose tissue

c The major regions and zones of an adrenal gland and the hormones they produce

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 Adrenal Medulla

• Medullary chromaffin cells synthesize

epinephrine (80%) and norepinephrine (20%)
• Effects
• Vasoconstriction
• Increased heart rate
• Increased blood glucose levels
• Blood diverted to brain, heart, and skeletal muscle
• Effects are relatively brief

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 Adrenal Medulla

• Responses brief
• Epinephrine stimulates
• metabolic activities,
• bronchial dilation, and
• blood flow to skeletal muscles & heart – vasodilation
• smooth muscles of bronchi and certain arteries relax

• Norepinephrine influences peripheral

vasoconstriction and blood pressure

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 18-6 Adrenal Glands

• Epinephrine and Norepinephrine

• Activation of the adrenal medullae has the
following effects:
• In the liver & skeletal muscle, glycogen molecules
are broken down
• The resulting glucose molecules are released
into the bloodstream
• Primarily for use by neural tissue, which cannot shift
to fatty acid metabolism
• In the heart, the stimulation of beta 1 receptors
triggers an increase in the rate and force of
cardiac muscle contraction

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 Figure 16.17 Stress and the adrenal gland.

Short-term stress Prolonged stress

Stress

Nerve impulses Hypothalamus

CRH (corticotropin-
releasing hormone)

Spinal cord

Corticotropic cells
of anterior pituitary
Preganglionic To target in blood
sympathetic
fibers
Adrenal cortex
Adrenal medulla (secretes steroid
(secretes amino acid– hormones)
based hormones) ACTH

Catecholamines
Mineralocorticoids Glucocorticoids
(epinephrine and
norepinephrine)
Short-term stress response Long-term stress response
• Heart rate increases • Kidneys retain • Proteins and fats converted
• Blood pressure increases sodium and water to glucose or broken down
• Bronchioles dilate • Blood volume and for energy
• Liver converts glycogen to glucose and releases blood pressure • Blood glucose increases
glucose to blood rise • Immune system
• Blood flow changes, reducing digestive system activity supressed
and urine output
• Metabolic rate increases

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 Pineal Gland

• Small gland hanging from roof of third ventricle

• Pinealocytes secrete melatonin, derived from
serotonin
• Melatonin may affect
• Timing of sexual maturation and puberty
• Day/night cycles circadian rhythms
• Physiological processes that show rhythmic variations
(body temperature, sleep, appetite)
• Production of antioxidant and detoxification molecules
in cells

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Figure 18-16a The Pancreas.

Pancreas
Pancreatic Body of Lobule Tail
Common duct pancreas
bile duct

Accessory
pancreatic
duct

Head of
pancreas

Small
intestine
(duodenum)

a The gross anatomy of the pancreas

Contains exocrine and

endocrine cells
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Figure 18-16b The Pancreas.

Pancreatic acini
(clusters of
exocrine cells)

Pancreatic islet
(islet of Langerhans)

Capillary

Pancreatic islet LM × 400

b A pancreatic islet surrounded

by exocrine cells

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© 2013 Pearson Education, Inc.

Pancreas

• Triangular gland partially behind stomach

• Has both exocrine and endocrine cells
• Acinar cells (exocrine) produce enzyme-rich juice
for digestion – essential for nutrient breakdown
and absorption
• Pancreatic islets (islets of Langerhans) contain
endocrine cells
• Alpha () cells produce glucagon (hyperglycemic
hormone)
• Beta () cells produce insulin (hypoglycemic
hormone)

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 Glucagon – alpha cells
increase blood glucose
• Major target—liver
• Produced by alpha cells
• Effects
• Glycogenolysis—breakdown of glycogen to
glucose in muscle & liver
• Gluconeogenesis—synthesis of glucose from
lactic acid and noncarbohydrates
• Release of glucose to blood
• Stimulate breakdown of triglycerides in adipose
tissue

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 Insulin – beta cells, lower blood glucose
• Major target – muscle, adipose, liver, most cells
• Enhances membrane transport of glucose
• Increases number of transporters
• Facilitated diffusion
• Accelerates glucose utilization – activating key
enzymes in glycolysis
• Anabolic: stimulates amino acid transport & protein
synthesis
• Inhibits glycogenolysis and gluconeogenesis &
stimulates glycogen formation
• Liver, skeletal muscles
• Stimulates triglyceride formation by adipose
• Insulin independent glucose uptake: liver, kidney, brain,
©
digestive tract, erythrocytes(RBC’s)
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 Factors That Influence Insulin Release

• Elevated blood glucose levels – primary

stimulus
• Rising blood levels of amino acids and fatty acids
• Release of acetylcholine by parasympathetic
nerve fibers
• Hormones glucagon, epinephrine, growth
hormone, thyroxine, glucocorticoids
• Somatostatin; sympathetic nervous system

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Figure 18-17 The Regulation of Blood Glucose Concentrations (Part 1 of 2).

Increased rate of
glucose transport into
target cells

Increased rate of
glucose utilization
and ATP generation

Increased conversion of
glucose to glycogen

Increased amino acid

absorption and
protein synthesis

Beta cells Increased triglyceride

Increasing blood glucose levels

secrete synthesis in adipose

insulin tissue

HOMEOSTASIS
RESTORED
HOMEOSTASIS
DISTURBED Blood glucose
levels decrease
Increasing blood
glucose levels

HOMEOSTASIS
Normal blood
glucose levels
(70–110 mg/dL)

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Figure 18-17 The Regulation of Blood Glucose Concentrations (Part 2 of 2).

HOMEOSTASIS

Decreasing blood glucose levels

Normal blood
glucose levels
(70–110 mg/dL)

HOMEOSTASIS
DISTURBED
HOMEOSTASIS
Decreasing blood RESTORED
glucose levels
Blood glucose
levels increase

Alpha cells
secrete
glucagon
Increased breakdown of
glycogen to glucose (in
liver, skeletal muscle)

Increased breakdown
of fat to fatty acids (in
adipose tissue)

Increased synthesis
and release of
glucose (by the liver)
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Table 18-5 Hormones Produced by the Pancreatic Islets.

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 18-8 Pancreas

• Diabetes Mellitus
• Is characterized by glucose concentrations high
enough to overwhelm the reabsorption capabilities
of the kidneys
• Hyperglycemia  abnormally high glucose levels
in the blood in general
• Glucose appears in the urine, and urine volume
generally becomes excessive (polyuria)

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 Diabetes Mellitus: Signs

• Three cardinal signs of DM

• Polyuria—huge urine output
• Glucose acts as osmotic diuretic
• Polydipsia—excessive thirst
• From water loss due to polyuria
• Polyphagia—excessive hunger and food
consumption
• Cells cannot take up glucose; are "starving"

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 18-8 Pancreas

• Diabetes Mellitus
• Type 1 (insulin dependent) diabetes
• Is characterized by inadequate insulin production
by the pancreatic beta cells
• Persons with type 1 diabetes require insulin to live
and usually require multiple injections daily, or
continuous infusion through an insulin pump or
other device
• This form of diabetes accounts for only around
5–10 percent of cases; it often develops in
childhood

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 18-8 Pancreas

• Diabetes Mellitus
• Type 2 (non-insulin dependent) diabetes
• Is the most common form of diabetes mellitus
• Most people with this form of diabetes produce
normal amounts of insulin, at least initially, but their
tissues do not respond properly, a condition known
as insulin resistance
• Type 2 diabetes is associated with obesity
• Weight loss through diet and exercise can be an
effective treatment

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 18-8 Pancreas

• Diabetes Mellitus
• Complications of untreated, or poorly managed
diabetes mellitus include:
• Kidney degeneration
• Retinal damage
• Early heart attacks
• Peripheral nerve problems
• Peripheral tissue damage

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 18-9 Endocrine Tissues of Other Systems

• The Intestines
• Produce hormones important to coordination
of digestive activities

• The Kidneys
• Produce the hormones calcitriol and
erythropoietin (EPO)
• Produce the enzyme renin

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Figure 18-19a Endocrine Functions of the Kidneys.

Sunlight Digestive
tract

Cholesterol
Epidermis

Cholecalciferol
Dietary
cholecalciferol
Liver

Parathyroid glands
Intermediate
form

Stimulation of
PTH
calcium and
phosphate ion
Calcitriol absorption
Kidney

a The production of calcitriol

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Figure 18-19b Endocrine Functions of the Kidneys.

HOMEOSTASIS

Normal
blood pressure
and volume
HOMEOSTASIS HOMEOSTASIS
DISTURBED RESTORED

Falling blood Rising blood

pressure and volume pressure and
volume
Kidney

Falling renal
blood flow Increased
fluid intake
and O2
and retention
Increased
Erythropoietin red blood cell
production Aldosterone
released
secreted

Renin released ADH secreted

ACE Stimulation of
Angiotensin II thirst
Angiotensinogen Angiotensin I

b The release of renin and erythropoietin, and an overview of the renin-

angiotensin-aldosterone system beginning with the activation of
angiotensinogen by renin
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 18-9 Endocrine Tissues of Other Systems

• The Heart
• Produces natriuretic peptides (ANP and BNP)
• When blood volume becomes excessive
• Action opposes angiotensin II
• Resulting in reduction in blood volume and blood
pressure

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 18-9 Endocrine Tissues of Other Systems

• The Thymus
• Produces thymosins (blend of thymic hormones)
• That help develop and maintain normal immune
defenses

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 18-9 Endocrine Tissues of Other Systems

• The Gonads endocrine tissue + gametogenesis

• Testes
• Produce androgens in interstitial cells
• Testosterone is the most important male hormone
• Supports male sexual characteristics
• Testosterone + FSH supports gametes
• Converted to DHT (dihydrotestosterone) in tissues
• Negative feedback GnRH, LH

• Produce inhibin in nurse cells

• Nurse cells support differentiation and physical maturation
of sperm
• Negative feedback with FSH
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 18-9 Endocrine Tissues of Other Systems
• The Gonads
• Ovaries
• Follicle cells produce estrogens
• Principal estrogen is estradiol
• Complicated feed back with LH & FSH
• Both negative & positive feedback depending on
time of the cycle
• Inhibin –FSH negative feedback
• Supports female sex characteristics and oogenesis
(make ova)

• After ovulation, follicle cells:

• Reorganize into corpus luteum
• Release estrogens and progestins, especially
progesterone - pregnancy
• Negative feedback with LH
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Table 18-7 Hormones of the Reproductive System.

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 18-9 Endocrine Tissues of Other Systems

• Adipose Tissue Secretions

• Leptin
• Feedback control for appetite
• Controls normal levels of GnRH, gonadotropin
synthesis

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Table 18-6 Representative Hormones Produced by Organs of Other Systems.

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 18-10 Hormone Interactions

• Hormones Important to Growth

• Growth hormone (GH)
• Thyroid hormones
• Insulin
• PTH and calcitriol
• Reproductive hormones

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 18-10 Hormone Interactions
• Growth Hormone (GH)
• In children:
• Supports muscular and skeletal development
• In adults:
• Maintains normal blood glucose concentrations
• Mobilizes lipid reserves

Thyroid Hormones
If absent during fetal development or for first year:
Nervous system fails to develop normally
Mental retardation results
If T4 concentrations decline before puberty:
Normal skeletal development will not continue

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 18-10 Hormone Interactions

• Insulin
• Allows passage of glucose and amino acids
across plasma membranes

• Parathyroid Hormone (PTH) and Calcitriol

• Promote absorption of calcium salts for deposition
in bone
• Inadequate levels cause weak and flexible bones

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 18-10 Hormone Interactions

• Reproductive Hormones
• Androgens in males, estrogens in females
• Stimulate cell growth and differentiation in target
tissues
• Produce gender-related differences in:
• Skeletal proportions
• Secondary sex characteristics

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 Endocrine Disorders
• Can result from disorder of gland
• Tumor, damage, malformation
• Can result from breakdown of control system
• Can result from malfunction of receptors on
target cells
• Hypersecretion
• Results in higher than normal level of hormone
• Hyposecretion
• Results in lower than normal level of hormone

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 18-10 Hormone Interactions

• The Hormonal Responses to Stress

• General Adaptation Syndrome (GAS)
• Also called stress response
• How body responds to stress-causing factors
• Is divided into three phases
1. Alarm phase
2. Resistance phase
3. Exhaustion phase

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Figure 18-20 The General Adaptation Syndrome (Part 1 of 3).

Alarm Phase (“Fight or Flight”)

During the alarm phase, an immediate

response to the stress occurs. Immediate Short-Term
The sympathetic division of Brain Responses to Crises
the autonomic nervous General
sympathetic • Increased mental alertness
system directs this activation • Increased energy use by all
response. In the alarm cells
phase, (1) energy • Mobilization of glycogen and
reserves are mobilized, Adrenal medulla lipid reserves
mainly in the form of Sympathetic • Changes in circulation
glucose, and (2) the body stimulation • Decreased digestive activity
prepares to deal with the Epinephrine, and urine production
stress-causing factor by “fight or flight” norepinephrine • Increased sweat gland
responses. Epinephrine is the dominant secretion
hormone of the alarm phase. Its secretion is • Increased heart rate and
respiratory rate
part of a generalized sympathetic activation.

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Figure 18-20 The General Adaptation Syndrome (Part 2 of 3).

Resistance Phase

If a stress lasts longer than a Long-Term Metabolic

few hours, the person enters Growth hormone
Adjustments
the resistance phase of
GAS. Glucocorticoids are Pancreas • Mobilization of remaining
the dominant hormones Glucagon energy reserves: Lipids are
of the resistance phase. released by adipose tissue;
Epinephrine, GH, and Sympathetic amino acids are released by
thyroid hormones are also stimulation skeletal muscle
• Conservation of glucose:
involved. Energy demands in the
Peripheral tissues (except
resistance phase remain higher than ACTH Adrenal cortex neural) break down lipids to
normal, due to the combined effects of obtain energy
these hormones. Neural tissue has a high • Elevation of blood glucose
demand for energy, and requires a reliable Glucocorticoids
concentrations: Liver
supply of glucose. If blood glucose levels synthesizes glucose from
fall too low, neural function deteriorates. Kidney other carbohydrates, amino
Glycogen reserves can meet neural demand Mineralocorticoids acids, and lipids
(with ADH) • Conservation of salts and
during the alarm phase, but become
depleted after several hours. Hormones of water, loss of K+ and H+
Renin-angiotensin-
the resistance phase mobilize lipids and aldosterone system
amino acids as energy sources to conserve
glucose for use by neural tissue.

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Figure 18-20 The General Adaptation Syndrome (Part 3 of 3).

Exhaustion Phase

The body’s lipid reserves are sufficient to maintain

Collapse of Vital Systems
the resistance phase for weeks or even months. But
when the resistance phase ends, homeostatic regu- • Exhaustion of lipid reserves
lation breaks down and the exhaustion phase • Cumulative structural or
begins. Unless corrective actions are taken almost functional damage to vital
immediately, the failure of one or more organ sys- organs
tems will prove fatal. The production of aldosterone • Inability to produce
throughout the resistance phase results in a conservation of Na+ at the expense of glucocorticoids
K+. As the body’s K+ content decreases, a variety of cells begin to malfunction. The • Failure of electrolyte balance
underlying problem of the exhaustion phase is the body’s inability to sustain the
endocrine and metabolic adjustments of the resistance phase.

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