ARTERIOLES

When an artery reaches the organ it is supplying, it branches into

numerous arterioles within the organ.
Explain how arteriolar radius can change and what impact this
would have on blood flow
- Arterioles are the major resistance vessel in the vascular tree
because their radius is small enough to offer considerable resistance to
flow.
- Blood flow from the artery to the arterioles (a drop in mean pressure)
helps establish the pressure differential that encourages the flow of
blood from the heart to the various organs downstream.
- The radius can be adjusted independently to accomplish two
functions: 1) to variably distribute the cardiac output among the
systemic organs, depending on the bodys momentary needs; and 2)
help regulate arterial blood pressure
- A smaller radius increases surface area that comes in contact with
blood
- Decreasing radius by results in a 16-fold increase in resistance

Discuss the local chemical and physical influences on arteriolar

radius
- Arteriolar walls contain very little elastic connective tissue; however,
they do have a thick later of smooth muscle that is innervated by
sympathetic nerve fibres
- The smooth muscle is sensitive to many local chemical changes and
to a few circulating hormones
- When the smooth muscle layer contracts, the vessels circumference
becomes smaller, increasing resistance and decreasing flow through
that vessel
Vasoconstriction: the narrowing of a vessel

Increased resistance
Decreased flow through vessel
Can be caused by
o Increased myogenic activity
o Increased oxygen
o Decreased CO2 and other metabolites
o Increased Endothelin
o Increased sympathetic stimulation, vasopressin, cold
Vasodilation: the enlargement in circumference and radius of vessel
Describe the sympathetic and parasympathetic control of
arteriolar radius
Arteriolar smooth muscle normally displays a state of partial
constriction known as vascular tone, which establishes a base line of
arteriolar resistance
- Two factors responsible for vascular tone a
o Arteriolar smooth muscle has considerable myogenic
activity; that is, its membrane potential fluctuates
independent of any neural or hormonal influences, leading
to self-induced contractile activity
o The sympathetic fibres supplying most arterioles
continually release norepinephrine, which further enhance
vascular tone
The ongoing tonic activity makes it possible to either increase or
decrease the level of contractile ability to accomplish vasoconstriction
or vasodilation. Were it not for tone, it would be impossible to reduce
the tension in an arteriolar wall to accomplish vasodilation; only
varying degrees of vasoconstriction would be possible
Discuss the interaction with local chemical control and
hormonal control of arteriolar radius
- Because blood is delivered to all organs at the same mean
arterial pressure, the driving force for flow is identical for each
organ. (total peripheral resistance/TPR is the summation of all
resistance vessels)
- Differences in flow to various organs are completely determined
by differences in the extent of vascularization and by
differences in resistance offered by the arterioles
supplying each organ.

Factors can influence

of contractile activity fall
into two categories:
1) Local (intrinsic) control,
are changes within an
organ that alter the radius
of the vessel and adjust
the blood flow by directly
affecting the smooth
muscles of the organs
arterioles (important in
determining the
distribution of cardiac
output)

levels

Local chemical influences: (are related to metabolic changes within a

given organ)
- Metabolic change (following factors produce relaxation of
arteriolar smooth muscles active hyperaemia)
o Decreased oxygen
o Decreased ATP
o Increase CO2
o Increased acid
o Increased K+
o Increased osmolality
o Adenosine and prostaglandin release
- Vasoactive mediators
o Endothelial cells, a single layer of specialized epithelial
cells that line the lumen of all blood vessel, release
chemical mediators that play a key role in locally
regulating arteriolar caliber
o Endothelial cells release locally acting chemical
messengers in response to chemical changes in their
environment
o Among best studied local vasoactive mediator is nitric
oxide (NO), which causes local arteriolar vasodilation by
inducing relaxation of arteriolar smooth muscle in the
vicinity

Histamine release
o Is synthesized and stores within special connective tissue
cells in many organs and in certain types of circulating
white blood cells
o When organs are injured, histamine is release and acts as a
paracrine in the damaged region
o By promoting relation or arteriolar smooth muscles,
histamine is the major cause of vasodilation in an injured
area.

Local physical influences:

Local
application of

heat or cold

o o

Can

cause localized
arteriolar

vasodilation
Chemical response to shear stress
o Because of friction, blood flowing over the surface of the
vessel lining creates a longitudinal force known as sheer
stress on the endothelial cells. Increase in sheer stress
causes the endothelial cells to release nitric oxide, which
diffuses to the underlying smooth muscle and promotes
vasodilation.
Myogenic response to stretch
o Arteriolar smooth muscle responds to being passively
stretched by myogenically increasing its tone via
vasoconstriction, thereby acting to resist the initial passive
stretch.

o Myogenic responses, coupled with metabolically induced

responses, are important in reactive hyperaemia and auto
regulation.
HYPEREMIA

AUTO-REGULATION
- Local mechanisms that keep tissue blood flow fairly constant
despite rather wide deviations in mean arterial driving pressure
- When mean arterial pressure falls, the driving force is reduced,
so blood flow to organs decrease
- The resultant changes in local metabolites and the reduces
stretch in the arterioles collectively brings about arteriolar
dilation to help restore tissue blood flow to normal despite the
reduced driving pressure
2) Extrinsic control, which are important in blood pressure regulation

Influence of total peripheral resistance

- To find the effect of changes in arteriolar resistance on mean
arterial pressure, the formula F = change in P / R applies to the
entire circulation as well as to a single vessel
Norepinephrines influence on smooth muscle
- The norepinephrine released from sympathetic nerve endings
combines with a-adrenergic receptors on arteriolar smooth
muscle to bring about vasoconstriction.
- Except cerebral arterioles, because brain blood flow must remain
constant to meet the brains continual need for oxygen
- Sympathetic activity contributes in an important way to
maintaining mean arterial pressure, ensuring an adequate
driving force for blood flow to the brain at the expense of organs
that can better withstand reduced blood flow
- Other organs that really need additional blood, such as active
muscles, obtain it thought local controls that override the
sympathetic effect
Local controls override sympathetic vasoconstriction
- Skeletal and cardiac muscles have the most powerful local
control mechanisms with which to override generalized
sympathetic vasoconstriction.
No parasympathetic innervation to arterioles
- There is no significant parasympathetic innervation to arterioles,
with the exception of the abundant parasympathetic vasodilator
supply to the arterioles of the penis and clitoris
- The rapid, profuse vasodilation induced by parasympathetic
stimulation in these organs (by means of promoting release of
NO) is largely responsible for accomplishing erection
- Decreasing sympathetic vasoconstrictor activity below tonic level
elsewhere produces vasodilation. When mean pressure rising
above normal, reflex reduction in sympathetic vasoconstrictor
activity accomplishes generalized arteriolar vasodilation to help
bring the driving pressure down to normal
- The main region of the brain that adjust sympathetic output to the
arterioles is the cardiovascular control center in the medulla of the
brain stem.
- Several hormones also extrinsically influence arteriolar radius
- Epinephrine and norepinephrine, which generally reinforce the
sympathetic nervous system
Vasopressin and angiotensin II, which are important in controlling
fluid balance and are potent vasoconstrictors