The Cardiovascular System: Blood Vessels
Fluctuations in systemic blood pressure would cause problems
for individual organs were it not for the
origin) of vascular smooth muscle. In-
adequate blood perfusion through an organ is quickly followed
by a decline in the organ’s metabolic rate and, if prolonged, or-
gan death. Likewise, excessively high arterial pressure and tis-
sue perfusion can be dangerous because the combination may
rupture more fragile blood vessels.
Fortunately, vascular smooth muscle prevents these prob-
lems by responding directly to passive stretch (caused by in-
creased intravascular pressure) with increased tone, which
resists the stretch and causes vasoconstriction. Reduced stretch
promotes vasodilation and increases blood ﬂow into the tissue.
Tese myogenic responses keep tissue perfusion fairly constant
despite most variations in systemic pressure.
Generally, both metabolic and myogenic factors determine the
ﬁnal autoregulatory response of a tissue. For example,
me-ah) refers to the dramatically increased
blood ﬂow into a tissue that occurs a±er the blood supply to the
area has been temporarily blocked. It results both from the myo-
genic response and from the metabolic wastes that accumulated in
the area during occlusion.
summarizes the various
intrinsic (local) and extrinsic controls of arteriolar diameter.
If a tissue needs more nutrients than short-term autoregulatory
mechanisms can supply, a long-term autoregulatory mechanism
may develop over weeks or months to enrich local blood ﬂow still
more. Te number of blood vessels in the region increases, and
existing vessels enlarge. Tis phenomenon, called
particularly common in the heart when a coronary vessel is par-
tially occluded. It occurs throughout the body in people who live
in high-altitude areas, where the air contains less oxygen.
Blood Flow in Special Areas
Each organ has special requirements and functions that are re-
vealed in its pattern of autoregulation. Autoregulation in the
brain, heart, and kidneys is extraordinarily eﬃcient, maintain-
ing adequate perfusion even when MAP ﬂuctuates.
Blood ﬂow in skeletal muscle varies with ﬁber type and muscle
activity. Generally speaking, capillary density and blood ﬂow are
greater in red (slow oxidative) ﬁbers than in white (fast glycolytic)
ﬁbers. Resting skeletal muscles receive about 1 L of blood per
minute, and only about 25% of their capillaries are open. During
rest, myogenic and general neural mechanisms predominate.
When muscles become active, blood ﬂow increases (
) in direct proportion to their greater
. Tis form
of autoregulation occurs almost entirely in response to the de-
creased oxygen concentration and accumulated metabolic factors
that result from the “revved-up” metabolism of working muscles.
as needed to maintain that constant pressure. Changes in blood
ﬂow through individual organs are controlled
modifying the diameter of local arterioles feeding the capillaries.
You can compare blood ﬂow autoregulation to water use in
your home. ²o get water in a sink or a garden hose, you have to
turn on a faucet. Whether you have several taps open or none,
the pressure in the main water pipe in the street remains rela-
tively constant, as it does in the even larger water lines closer to
the pumping station. Similarly, local conditions in the arterioles
feeding the capillary beds of an organ have little eﬀect on pres-
sure in the muscular artery feeding that organ, or in the large
elastic arteries. Te pumping station is, of course, the heart. Te
beauty of this system is that as long as the water company (cir-
culatory feedback mechanisms) maintains a relatively constant
water pressure (MAP), local demand regulates the amount of
ﬂuid (blood) delivered to various areas.
In summary, organs regulate their own blood ﬂows by vary-
ing the resistance of their arterioles. As we describe next, these
intrinsic control mechanisms may be classed as
When blood ﬂow is too low to meet a tissue’s metabolic needs,
oxygen levels decline and metabolic products (which act as
paracrines) accumulate. Tese changes serve as autoregulation
stimuli that lead to automatic increases in tissue blood ﬂow.
Te metabolic factors that regulate blood ﬂow are low oxy-
gen levels, and increases in H
and lactic acid), K
adenosine, and prostaglandins. Te relative importance of these
factors is not clear. Many of them act directly to relax vascular
smooth muscle, but some may act by causing vascular endothe-
lial cells to release nitric oxide.
Nitric oxide (NO)
is a powerful vasodilator which acts via a
cyclic GMP second-messenger system. NO is quickly destroyed
and its potent vasodilator eﬀects are very brief. Even so, NO is
the major player in controlling local vasodilation, o±en over-
riding sympathetic vasoconstriction when tissues need more
Te endothelium also releases potent vasoconstrictors, in-
cluding the family of peptides called
, which are
among the most potent vasoconstrictors known. Normally, NO
and endothelin release from endothelial cells are in a dynamic
balance, but this balance tips in favor of NO when blood ﬂow is
too low for metabolic needs.
Te net result of metabolically controlled autoregulation is
immediate vasodilation of the arterioles serving the capillary
beds of the “needy” tissues and dilation of their precapillary
sphincters. Blood ﬂow to the area rises temporarily, allowing
blood to surge through the true capillaries and become available
to the tissue cells.
Inﬂammatory chemicals (such as histamine, kinins, and
prostaglandins) released in injury, infection, or allergic reac-
tions also cause local vasodilation. Inﬂammatory vasodilation
helps the defense mechanisms clear microorganisms and toxins
from the area, and promotes healing.