Chapter 12
active-hyperemia response in one or more organs. It is likely,
moreover, that additional important local factors remain to
be discovered. All these chemical changes in the extracellular
fl uid act locally upon the arteriolar smooth muscle, causing it
to relax. No nerves or hormones are involved.
It should not be too surprising that active hyperemia is
most highly developed in skeletal muscle, cardiac muscle, and
glands—tissues that show the widest range of normal meta-
bolic activities in the body. It is highly effi
cient, therefore, that
their supply of blood be primarily determined locally.
Flow Autoregulation
During active hyperemia, increased metabolic activity of the
tissue or organ is the initial event leading to local vasodila-
tion. However, locally mediated changes in arteriolar resis-
tance can also occur when a tissue or organ suffers a change
in its blood supply resulting from a change in blood pressure
Figure 12–34b
). The change in resistance is in the direction
of maintaining blood fl
ow nearly constant in the face of the
pressure change and is therefore termed
ow autoregulation.
For example, when arterial pressure in an organ is reduced,
say, because of a partial blockage in the artery supplying the
organ, local controls cause arteriolar vasodilation, which tends
to maintain relatively constant fl ow.
What is the mechanism of fl ow autoregulation? One
mechanism comprises the same metabolic factors described
for active hyperemia. When an arterial pressure reduction low-
ers blood fl ow to an organ, the supply of oxygen to the organ
diminishes, and the local extracellular oxygen concentration
decreases. Simultaneously, the extracellular concentrations of
carbon dioxide, hydrogen ions, and metabolites all increase
because the blood cannot remove them as fast as they are
produced. Also, eicosanoid synthesis is increased by unclear
stimuli. Thus, the local metabolic changes occurring dur-
ing decreased blood supply at constant metabolic activity are
similar to those that occur during increased metabolic activ-
ity. This is because both situations refl ect an initial imbalance
between blood supply and level of cellular metabolic activity.
Note, then, that the vasodilations of active hyperemia and of
fl ow autoregulation in response to low arterial pressure do not
differ in their major mechanisms, which involve local meta-
bolic factors, but in the event—altered metabolism or altered
blood pressure—that brings these mechanisms into play.
Flow autoregulation is not limited to circumstances in
which arterial pressure decreases. The opposite events occur
when, for various reasons, arterial pressure increases: The ini-
tial increase in fl ow due to the increase in pressure removes the
local vasodilator chemical factors faster than they are produced
and also increases the local concentration of oxygen. This
causes the arterioles to constrict, thereby maintaining a rela-
tively constant local fl ow in the face of the increased pressure.
Although our description has emphasized the role of
local chemical factors in fl
ow autoregulation, another mecha-
nism also participates in this phenomenon in certain tissues
and organs. Some arteriolar smooth muscle responds directly
to increased stretch, caused by increased arterial pressure, by
contracting to a greater extent. Conversely, decreased stretch,
due to decreased arterial pressure, causes this vascular smooth
muscle to decrease its tone. These direct responses of arterio-
lar smooth muscle to stretch are termed
myogenic responses.
They are caused by changes in calcium movement into the
smooth muscle cells through stretch-sensitive calcium chan-
nels in the plasma membrane.
Reactive Hyperemia
When an organ or tissue has had its blood supply completely
occluded, a profound transient increase in its blood fl ow
occurs as soon as the occlusion is released. This phenomenon,
known as
reactive hyperemia,
is essentially an extreme form
of fl ow autoregulation. During the period of no blood fl ow,
the arterioles in the affected organ or tissue dilate, owing to
the local factors described previously. Blood fl ow, therefore,
increases greatly through these wide-open arterioles as soon
as the occlusion to arterial infl
ow is removed. This effect can
be demonstrated by wrapping a string tightly around the base
of your fi
nger for several minutes. When it is removed, your
fi nger will turn bright red due to the increase in blood fl ow.
Response to Injury
Tissue injury causes a variety of substances to be released
locally from cells or generated from plasma precursors. These
substances make arteriolar smooth muscle relax and cause
vasodilation in an injured area. This phenomenon, a part of
the general process known as infl ammation, will be described
in detail in Chapter 18.
Extrinsic Controls
Sympathetic Nerves
Most arterioles receive a rich supply of sympathetic postgan-
glionic nerve fi bers. These neurons release mainly norepineph-
rine, which binds to alpha-adrenergic receptors on the vascular
smooth muscle to cause vasoconstriction.
In contrast, recall that the receptors for norepinephrine
on heart muscle, including the conducting system, are mainly
beta-adrenergic. This permits the pharmacologic use of beta-
adrenergic antagonists to block the actions of norepinephrine
on the heart but not the arterioles, and vice versa for alpha-
adrenergic antagonists.
Control of the sympathetic nerves to arterioles can also be
used to produce vasodilation. Because the sympathetic nerves
are seldom completely quiescent but discharge at some inter-
mediate rate that varies from organ to organ, they always are
causing some degree of tonic constriction in addition to the
vessels’ intrinsic tone. Dilation can be achieved by decreasing
the rate of sympathetic activity below this basal level.
The skin offers an excellent example of the role the sym-
pathetic nerves play. At room temperature, skin arterioles are
already under the infl uence of a moderate rate of sympathetic
discharge. An appropriate stimulus—cold, fear, or loss of blood,
for example—causes refl ex enhancement of this sympathetic
discharge, and the arterioles constrict further. In contrast, an
increased body temperature refl exively inhibits the sympathetic
nerves to the skin, the arterioles dilate, and the skin fl ushes as
you radiate body heat.
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