Cardiovascular Physiology
403
SECTION C SUMMARY
Arteries
I. The arteries function as low-resistance conduits and as pressure
reservoirs for maintaining blood fl ow to the tissues during
ventricular relaxation.
II. The difference between maximal arterial pressure (systolic
pressure) and minimal arterial pressure (diastolic pressure)
during a cardiac cycle is the pulse pressure.
III. Mean arterial pressure can be estimated as diastolic pressure
plus one-third pulse pressure.
Arterioles
I. Arterioles, the dominant site of resistance to fl ow in the
vascular system, play major roles in determining mean arterial
pressure and in distributing fl ows to the various organs and
tissues.
II. Arteriolar resistance is determined by local factors and by refl ex
neural and hormonal input.
a. Local factors that change with the degree of metabolic
activity cause the arteriolar vasodilation and increased fl ow
of active hyperemia.
b. Flow autoregulation, a change in resistance that maintains
a constant fl ow in the face of changing arterial blood
pressure, is due to local metabolic factors and to arteriolar
myogenic responses to stretch.
c. The sympathetic nerves, which innervate most arterioles,
cause vasoconstriction via alpha-adrenergic receptors. In
certain cases, noncholinergic, nonadrenergic neurons that
release nitric oxide or other noncholinergic vasodilators also
innervate blood vessels.
d. Epinephrine causes vasoconstriction or vasodilation,
depending on the proportion of alpha- and beta-2
adrenergic receptors in the organ.
e. Angiotensin II and vasopressin cause vasoconstriction.
f. Some chemical inputs act by stimulating endothelial cells
to release vasodilator or vasoconstrictor paracrine agents,
which then act on adjacent smooth muscle. These paracrine
agents include the vasodilators nitric oxide (endothelium-
derived relaxing factor) and prostacyclin, and the
vasoconstrictor endothelin-1.
III. Table 12–5 summarizes arteriolar control in specifi c organs.
Capillaries
I. Capillaries are the site where nutrients and waste products are
exchanged between blood and tissues.
II. Blood fl ows through the capillaries more slowly than through
any other part of the vascular system because of the huge
cross-sectional area of the capillaries.
III. Capillary blood fl ow is determined by the resistance of the
arterioles supplying the capillaries and by the number of open
precapillary sphincters.
IV. Diffusion is the mechanism that exchanges nutrients and
metabolic end products between capillary plasma and
interstitial fl
uid.
a. Lipid-soluble substances move across the entire endothelial
wall, whereas ions and polar molecules move through
water-fi lled intercellular clefts or fused-vesicle channels.
b. Plasma proteins move across most capillaries only very
slowly, either by diffusion through water-fi lled channels or
by vesicle transport.
c. The diffusion gradient for a substance across capillaries
arises as a result of cell utilization or production of the
substance. Increased metabolism increases the diffusion
gradient and increases the rate of diffusion.
V. Bulk fl ow of protein-free plasma or interstitial fl uid across
capillaries determines the distribution of extracellular fl
uid
between these two fl
uid compartments.
a. Filtration from plasma to interstitial fl uid is favored by the
hydrostatic pressure difference between the capillary and
Causes of Edema
In addition to the blockage of lymph return discussed
previously, other disease states produce edema by affecting
one or more of the Starling forces.
Heart failure is a condition in which elevated venous
pressure backs blood up into the capillaries, and the elevated
hydrostatic pressure (
P
c
) causes fi ltration to occur faster than
the lymphatics can remove interstitial fl uid. The resulting
edema can occur in either systemic or pulmonary capillary
beds, as we will discuss in an upcoming section.
A more common experience is the swelling that
occurs with injury—for example, when you sprain an ankle.
Histamine, along with other chemical factors released
locally in response to injury, dilate arterioles and thus
elevate capillary pressure and fi ltration (review Figures 12–42
and 12–43). In addition, the chemicals released within
injured tissue cause endothelial cells to distort, increasing
ADDITIONAL CLINICAL EXAMPLES
the size of intercellular clefts and allowing plasma proteins
to escape from the bloodstream more readily. This increases
the protein osmotic force in the interstitial fl
uid (
π
IF
),
adding to the tendency for fi ltration and edema to occur.
Finally, an abnormal decrease in plasma protein
concentration also can result in edema. This condition
reduces the main absorptive force at capillaries (
π
c
), thus
allowing an increase in net fi ltration. Plasma protein
concentration can be reduced by liver disease (decreased
plasma protein production) or by kidney disease (loss of
protein in the urine). In addition, as with liver disease,
protein malnutrition
(
kwashiorkor
)
compromises the
manufacture of plasma proteins. The resulting edema is
particularly marked in the interstitial spaces within the
abdominal cavity, producing the swollen-belly appearance
commonly observed in people with insuffi cient protein in
their diets.
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