dr. Nuraiza Meutia,M.

Biomed
Departemen Fisiologi FK USU
 2

 Aktivitas saluran cerna untuk menjalankan

proses percernaan diatur oleh sistem saraf dan
endokrin.
 Saluran cerna memiliki kemandirian untuk
kedua sistem tersebut.
 Terjadi aktivitas terintegrasi antara kedua
sistem  mengatur aktivitas motorik dan
sekretorik
 3
Pada akhir perkuliahan, anda harus dapat :
1. Menjelaskan anatomi fungsional dinding GIT
2. Menjelaskan aktivitas utama GIT
3. Menjelaskan persarafan otonom yang mengatur GIT
4. Menjelaskan letak dan fungsi pleksus saraf di GIT
5. Menyebutkan nama dan efek neurotransmitter yang bekerja di ENS
6. Menjelaskan peran hormon dalam kontrol GIT (nama hormon,
sumber, target dan efek)
7. Menjelaskan proses integrasi sistem saraf dan endokrin di GIT
8. Menjelaskan perbedaan refleks lokal dan refleks sentral dalam
regulasi kerja GIT
9. Menjelaskan aktivitas listrik pada otot polos GIT
10. Menjelaskan mekanisme kontraksi dan jenis motilitas GIT
11. Menjelaskan contoh-contoh refleks GI
12. Menjelaskan regulasi aktivitas lambung, usus halus, usus besar,
pankreas dan kandung empedu.
 4
Struktur Dinding GIT
 5

 Aktivitas GIT :

Motilitas

Sekresi

Digesti

Absorbsi
 6

Fungsi sistem regulasi di GIT :

 Mengatur aktivitas motilitas dan sekresi

 Mengatur aliran darah ke GIT
 Menerima dan menyampaikan informasi
melalui neuron sensori (aferen) , dari
reseptor-reseptor yang menerima stimulus
mekanikal, thermal, osmotik dan kimiawi.
 7

GIT NEURAL
CONTROL
 8

 Terdiri dari :
- Divisi parasimpatetik
- Divisi simpatetik
- Enteric Nervous System (ENS)
 9

 Parasimpatetik

N. Vagus & N.pelvik

Neuron preganglionik panjang; postganglionik
pendek, bersinaps dengan neuron ENS

Stimulasi  eksitasi aktivitas ENS

Mengandung serat sensori aferen (80 %)

N.Vagus bersinaps ke neuron ENS di esophagus,
lambung,usus halus, sebagian kolon, kandung
empedu, & pankreas

N.Pelvik bersinaps dengan ENS di usus besar

Neurotransmitter : Ach
 10

Parasympathetic

Nervous System
Craniosacral
 11

 Simpatetik

 Serat simpatetik ke GIT berasal dari

medula spinalis segmen T-5 sampai L-2.
 Neurotransmitter : norepinefrin
 Aktivitas simpatetik  inhibisi motilitas
dan sekresi GIT, konstriksi sfinkter dan
pembuluh darah.
 12

Sympathetic
Nervous
System
Thoracolumbar
 13

Enteric Nervous System

 Enteric Nervous System (ENS) terdapat di seluruh dinding GIT,
mulai esophagus sampai anus.
 Terbentuk dari 100 juta neuron (mengimbangi spinal cord).
 Memiliki 3 jenis neuron : sensori, motorik, & interneuron
 ENS tersusun atas 2 pleksus utama :
(1) Myenteric plexus atau Auerbach's Plexus: berada di antara
lapisan otot sirkular dan longitudinal (outer plexus). Fungsi :
mengontrol motilitas GIT
(2) Submucosal Plexus atau Meissner's plexus : berada di
lapisan submukosa (inner plexus). Fungsi : mengatur sekresi dan
aliran darah lokal, sensing perubahan lumen, dan gerak pelipatan
mukosa.
14
 15

 ENS dapat berfungsi secara mandiri, terlepas dari

pengaturan sistem simpatetik dan parasimpatetik.
 Meskipun, persarafan ekstrinsik dapat sangat
mempengaruhi ENS, menyebabkan inhibisi atau
eksitasi fungsi GIT.
 Ujung saraf sensori mengirimkan serat aferen ke
kedua pleksus ENS, dan juga ke : (1) ganglia
prevertebral sistem simpatetik, (2) spinal cord, dan
(3) nervus vagus menuju batang otak.
 Informasi sensorik dapat menimbulkan refleks lokal
dan sentral
16
 17

Figure 62-4; Guyton & Hall

 18

Neurotransmitters and Neuromodulators in the ENS

19
 20

GIT
HORMONAL
CONTROL
 21

 GIT merupakan kelenjar endokrin terbesar

 Hormon dihasilkan oleh sel enteroendokrin yang
tersebar di antara sel-sel epitel mukosa lambung dan
usus  Enteric Endocrine System.

 Sekresi hormon terjadi akibat stimuli tertentu, dan

berhenti bila stimuli lenyap.
 Sel-sel GIT menghasilkan regulator peptida, yang
berfungsi secara parakrin atau sebagai Nts, untuk
mempengaruhi motilitas, aliran darah, dan
pertumbuhan mukosa GIT.
 GIT Hormones 22

HORMONE ORIGIN STIMULUS ACTIONS

G cells of the stomach Small peptides and amino ↑ Gastric H+ secretion
acids Stimulates growth of gastric mucosa
Gastrin Distention of the stomach
Vagal stimulation (GRP)
I cells of the duodenum and Small peptides and amino ↑ Pancreatic enzyme secretion
jejunum acids ↑ Pancreatic HCO3- secretion
Fatty acids Stimulates contraction of the gallbladder and
Cholecystokinin (CCK) relaxation of the sphincter of Oddi
Stimulates growth of the exocrine pancreas
and gallbladder
Inhibits gastric emptying
S cells of the duodenum H+ in the duodenum ↑ Pancreatic HCO3- secretion
Fatty acids in the ↑ Biliary HCO3- secretion
Secretin duodenum ↓ Gastric H+ secretion
Inhibits trophic effect of gastrin on gastric
mucosa
Glucose-Dependent K cells of the Duodenum and Fatty acids ↑ Insulin secretion from pancreatic β cells
Insulinotropic Peptide jejunum Amino acids ↓ Gastric H+ secretion
Oral glucose
(GIP)
M cells of the duodenum and Fat Stimulates:
Motilin jejunum Acid Gastric motility
Nerve Intestinal motility
 23

GIT
NEURAL
HORMONAL CONTROL
INTEGRATION

Nervous and hormonal influences do not function

independently
- Neural activity  release of hormones
- Hormones  neural activity
- Simultaneous effects
 24

3 tipe refleks GI :
1. Refleks yang terintegrasi seluruhnya di dinding GIT (ENS):
mengatur sekresi dan motilitas secara lokal.
2. Refleks dari GIT  ke ganglia prevertebral simpatetik 
kembali ke GIT. Sehingga respon terjadi di bagian lain GIT.
Misal : r.gastrokolik, r.enterogastrik, & r.kolonoileal.
3. Refleks dari GIT  ke spinal cord atau batang otak  kembali
ke GIT.
Misalnya : (1) refleks dari lambung & duodenum ke Bt.otak,
kembali melalui N.Vagus untuk mengatur aktivitas sekresi dan
motorik lambung. (2)refleks nyeri yang mengakibatkan inhibisi
GIT.(3)refleks defekasi.
 25

Nerves
Reflex or
Hormone
secretion
 26

Regulasi Aliran Darah ke GIT

 Vasodilator : CCK, Secretin, Gastrin, VIP; kinin(kallidin &
bradykinin)
 Penurunan konsentrasi oksigen  peningkatan aliran darah
50-100 %
 Pengaruh persarafan otonom :

Stimulation of the Parasympathetic nerves going to the stomach and

lower colon increases local blood flow at the same time that it
increases glandular secretion.
Sympathetic stimulation, by contrast, has a direct effect on essentially all
the gastrointestinal tract to cause intense vasoconstriction of the
arterioles with greatly decreased blood flow. But the local metabolic
vasodilator mechanisms override the sympathetic vasoconstiction effects,
returning the normal blood flow to GI muscle and
glands...”autoregulatory escape”
 27

 Stres atau cemas dapat menginduksi : inhibisi aktivitas

saluran cerna bagian atas - dan stimulasi fungsi
motorik saluran cerna bagian bawah

 Disebabkan pengaruh corticotropin-releasing factor

(CRF) endogen terhadap reseptor CRF di sistem saraf
pusat.
 Interaksi CRF pada reseptor CRF-2 menyebabkan
inhibisi pengosongan lambung .
 Sedangkan reseptor CRF-1 berperan dalam
menghasilkan respon peningkatan motilitas kolon saat
stres.
 28

Aktivitas Listrik pada Otot polos GIT

 Di sepanjang otot polos GIT

terjadi fluktuasi potensial
membran sepanjang waktu.
 Perubahan potensial ini
menyebabkan otot polos
dapat berkontraksi.
 Aktivitas listrik ini 2 jenis :
(a) slow waves
(b) spikes.
 29

a. Slow Waves
 Bukan potensial aksi, fluktuasi depolarisasi dan repolarisasi .

 Amplitudo 5-15 mV

 Frekuensi berbeda di berbagai bagian GIT : lambung 3 x/mnt ;

duodenum 12 x/mnt; ileum terminal 8-9 x/mnt.

 Berperan untuk mensinkronkan irama kontraksi di sepanjang

GIT.
Origin of slow waves. They may
originate in the interstitial cells of Cajal
(the GI pacemaker), which are abundant in
the myenteric plexues. These interstitial
cells form a network with each other and
are interposed between the smooth muscle
layers, with synaptic-like contacts to
smooth muscle cells.
 30

Source of Slow Waves in GIT Muscles

 31

b. Spike Potential

 Apabila pada suatu tempat, potensial membran istirahat

meningkat, maka slow wave dapat mencetuskan potensial aksi
(spike potential)  kontraksi otot.
 Faktor yang dapat mendepolarisasi membran :
Peregangan otot
Ach
Stimulasi parasimpatetik
Stimulasi hormonal
 Faktor yang meng-hiperpolarisasi membran :
 Norepinephrine
 Stimulasi simpatetik
 32

Figure 62-3; Guyton & Hall

 33

 Peristalsis
Penjalaran gelombang
mendorong bolus

 Segmentasi
Gerakan mencampur
dan mengaduk bolus.
 Mass movements

 Peristaltik haustra

34
 35

 The main functions of the upper part of the

stomach (Reservoir part ):
1. To maintain a continuous compression
2. To accommodate the received food without significant
gastric wall distention or pressure (Storage of food)
 36

 Gastric secretion is controlled by both neural

and hormonal mechanisms
 Under normal conditions the gastric mucosa
creates as much as 3 liters of gastric juice
every day
 Gastric juice is an acid solution that has the
potential to dissolve nails
 37

 Nervous control is regulated by long (vagus

nerve mediated) and short (local enteric) nerve
reflexes
 When the vagus nerves actively stimulate the
stomach, secretory activity of virtually all of
its glands increase
 The sympathetic nerves depress secretory
activity
 38

 Hormonal control of gastric secretion is

largely from the presence of gastrin
 Gastrin stimulates the secretion of both
enzymes and HCL in the stomach
 Hormones produced by the small intestine are
largely gastrin antagonists
 39

 Stimuli acting at three distinct sites, the

head, stomach, and small intestine, provoke
or inhibit gastric secretory activity
 Accordingly the three phases are called
cephalic, gastric, and intestinal phases
 However, the effector site is the stomach in
all cases and once initiated, one or all
threephases may be occurring at the same
time
 40

 The cephalic reflex phase of gastric secretion

occurs before food enters the stomach
 It is triggered by the aroma, taste, sight, or
though of food
 During this phase the brain gets the stomach
ready for food
 41

 Inputs from activated olfactory receptors and

taste buds are relayed to the hypothalamus
which in turn stimulates the vagal nuclei of the
medulla oblongata, causing motor impulses to
be transmitted via the vagus nerves to the
parasympathetic nerve ganglia
 Eneteric ganglionic neurons in turn stimulate
the stomach glands
 42

 The enhanced secretory activity that results

when we see or think of food is a conditioned
reflex and occurs only when we like or want
the food
 If we are depressed or have no appetite, this
part of the cephalic reflex is suppressed
43
 44

 Once food reaches the stomach, local neural

and hormonal mechanisms initiate the gastric
phase
 This phase provides about two-thirds of the
gastric juice released
 The most important stimuli are distension,
peptids, and low acidity
 45

 Stomach distension activates stretch receptors

and initiates both local (myentertic) reflexes
and the long vagovagal reflexes
 In vagovagal reflex, impulses travel to the
medulla and then back to the stomach via
vagal fibers
 Both types of reflexes lead to acetylcholine
(ACH) release, which in turn stimulates the
output of more gastric juice by cells
 46

Figure 24.15b
 47

 Though neural influences initiated by

stomach distension are important, the
hormone gastrin probably plays a greater role
in stimulating stomach gland secretion during
the gastric phase
 Chemical stimuli provided by partially
digested proteins (peptids)caffine (colas,
coffee) and rising pH directly active gastrin
secreting entoendocrine cells called G cells
 48

 Although gastrin also stimulates the release of

enzymes, its main target is the HCL secreting
parietal cells, which it prods to spew out even
more HCL
 Highly acidic (pH below 2) gastric contents
inhibit gastrin secretion
 49

 When protein foods are in the stomach, the pH

of the gastric contents generally rises because
proteins act as buffers to tie up H +
 The rise in pH stimulates gastrin and
subsequently HCL release, which in turn
provides the acidic conditions needed for
protein digestion
 50

 The more protein in the meal, the greater the

amount of gastrin and HCL released
 As proteins are digested, the gastric contents
gradually become more acidic, which again
inhibits the gastrin secreting cells
 This negative feedback mechanism helps
maintain optimal pH and working conditions
for the gastric enzymes
 51

 G cells are also activated by the neural reflexes

already described
 Emotional upsets, fear, anxiety, or anything
that triggers the fight-or-flight response
inhibits gastric secretion because (during such
times) the sympathetic division overrides
parasympathetic controls of digestion
 52

 The control of the HCL secreting parietal cells

is unique and multifaceted
 Basically, HCL secretion is stimulated by three
chemicals, all of which work through second-
messenger systems Ach released by
parasympathetic nerve fibers and gastrin
secreted by G cells
 53

 Ach released by para-

sympathetic nerve
fibers and gastrin
secreted by G cells
bring about their
effects by increasing
intercellular Ca++
levels
 54

 Histamine
released by
mucosal cells
called
histaminocytes
acts through
cyclic AMP
(cAMP)
 55

 As hydrogen ions are secreted, chloride ions

(Cl-) are also pumped into the lumen to
maintain an electrical balance in the stomach
 The Cl- is obtained from blood plasma, while
the H+ appears to come from a breakdown of
carbonic acid formed by the combination of
carbon dioxide and water and within the
parietal cells
 56


CO2 + H2O  H2CO3
 H+ + HCO3-
 As H+ is pumped
from the cell and
HCO3- is ejected
through the basal cell
membrane into the
capillary blood
 57

 The result of ejection of the bicarbonate ion

into the capillary blood is that blood draining
from the stomach is more alkaline than the
blood serving it
 The phenomenon is called the alkaline tide
 58

 The intestinal phase of gastric secretion has

two components

One excitatory

One inhibitory
 59

 The excitatory aspect is set into motion as

partially digested food begins to fill the initial
part (duodenum) of the small intestine
 This stimulates intestinal mucosal cells to
release a hormone that encourages the gastric
glands to continue their secretory activity
 60

 The effects of this hormone imitate those of

gastrin, so it has been named intestinal
(enteric) gastrin
 However, intestinal mechanisms stimulate
gastrin secretion only briefly
 As the intestine distends with chyme
containing large amounts of H+, fats,
partially digested proteins, and irritating
substances, the inhibitatory component is
triggered in the form of the enterogastric
reflex
 61

 The enterogastric reflex is actually a trio of

reflexes that

Inhibit the vagal nuclei in the medulla

Inhibit local reflexes

Activate sympathetic fibers that cause the pyloric
sphincter to tighten and prevent further food entry
into the small intestine
 As a result, gastric secretory activity declines
 62

 These inhibitions on gastric activity product

the small intestine to harm due to excessive
acidity and match the small intestine’s
processing abilities to the amount of chyme
entering it at a given time
 63

 In addition, the factors just named trigger the release

of several intestinal hormones collectively called
enterogastrones which include

Secretin

Cholecystokinin (CCK)

Vasoactive intestinal peptide (VIP)

Gastric inhibitory peptide (GIP)

 All of these hormones inhibit gastric secretion when

the stomach is very active
 64

Figure 24.15c
 65

 Secretion of pancreatic juice is regulated both

by local hormones and by the parasympathetic
nervous system
 66

 Both hormones act on the pancreas, but secretin

targets the duct cells, prompting their release of
watery bicarbonate-rich pancreatic juice, Whereas
CCK stimulates the acini to release enzyme-rich
pancreatic juice

 Vagal stimulation causes release of pancreatic juice

primarily during the cephalic and gastric phases of
gastric secretion
 67

 Normally, the amount of HCL produced in the

stomach is exactly balanced by the amount of
bicarbonate (HCO3) actively secreted by the
pancreas
 HCO3 is secreted into the pancreatic juice, and H+
enters the blood
 Consequently, the pH of venous blood returning to
the heart remains relatively unchanged because
alkaline blood draining from the stomach is
neutralized by the acidic blood draining the
pancreas
 68

Regulation of Pancreatic Secretions

 Secretin

Acidity in intestines induces
Secretin release

Secretin releases pancreatic
Sodium Bicarbonate (HCO3-)
 CCK

Fats and proteins induce CCK
release

CCK releases pancreatic digestive
enzymes
 GIP

Fatty acids and sugar causes
induce GIP release

GIP induces insulin release
 69

 Although the liver makes bile continuously

bile does not usually enter the small intestine
until the gallbladder contract
 The major stimulus for gallbladder
contraction is the intestinal hormone
cholecystokinin (CCK)
 CCK is released to the blood when acidic,
fatty chyme enters the duodenum
 70

 Besides causing the gallbladder to contract, CCk

has two other important effects

It stimulates secreation of pancreatic juice

It relaxes the hepatppancreatic sphincter so that
bile and pancreatic juice can enter the
duodenum

 Parasympathetic impulses delivered by the vagus

nerves have a minor impact on stimulating
gallbladder contraction
 71

 The rectum is
usually empty, but
when feces are
forced into it by
mass movements,
stretching of the
rectal walls
initiates the
defecation reflex
 72

 This is a spinal
cord mediated
reflex that causes
the walls of the
sigmoid colon and
the rectum to
contract and the
anal sphincters to
relax
 73

 Distension or
stretch of the
rectal walls
triggers a
depolarization of
sensory (afferent)
fibers which
synapse with the
spinal cord
 74

 Parasympathetic
motor (efferent)
fibers, in turn,
stimulate
contraction of the
rectal walls and
relaxation of the
internal anal
sphincter
 75

 If it is convenient to
defecate, voluntary
signals stimulate the
relaxation of the
external anal
sphincter
 76

 As feces are forced into the anal canal, impulses reach

the brain allowing us to decide whether the
external(voluntary) anal sphincter should remain open
or closed
 If defection is delayed, the reflex contractions end
within a few seconds and the walls relax
 With the next mass movement, the reflex is initiated
again and again until one chooses to defecate