Cardiovascular Physiology
391
In contrast to active hyperemia and fl ow autoregulation,
the primary functions of sympathetic nerves to blood vessels
are concerned not with the coordination of local metabolic
needs and blood fl ow but with refl exes that serve whole body
“needs.” The most common refl ex employing these nerves is
that which regulates arterial blood pressure by infl uencing
arteriolar resistance throughout the body (discussed in detail
in the next section). Other refl exes redistribute blood fl ow
to achieve a specifi c function (as in the previous example, to
increase heat loss from the skin).
Parasympathetic Nerves
With few exceptions, there is little or no important parasym-
pathetic innervation of arterioles. In other words, the great
majority of blood vessels receive sympathetic but not parasym-
pathetic input. This contrasts with the pattern of dual auto-
nomic innervation seen in most tissues.
Noncholinergic, Nonadrenergic
Autonomic Neurons
As described in Chapter 6, there is a population of autonomic
postganglionic neurons that are labeled noncholinergic, non-
adrenergic neurons because they release neither acetylcholine
nor norepinephrine. Instead they release nitric oxide, a vaso-
dilator, and, possibly, other noncholinergic vasodilator sub-
stances. These neurons are particularly prominent in the enteric
nervous system, which plays a signifi cant role in the control of
the gastrointestinal system’s blood vessels (Chapter 15). These
neurons also innervate arterioles in certain other locations, for
example, in the penis, where they mediate erection.
Hormones
Epinephrine, like norepinephrine released from sympathetic
nerves, can bind to alpha-adrenergic receptors on arteriolar
smooth muscle and cause vasoconstriction. The story is more
complex, however, because many arteriolar smooth muscle
cells possess the beta-2 subtype of adrenergic receptors as well
as alpha-adrenergic receptors, and the binding of epinephrine
to beta-2 receptors causes the muscle cells to relax rather than
contract (
Figure 12–35
).
In most vascular beds, the existence of beta-2 adrenergic
receptors on vascular smooth muscle is of little if any impor-
tance because the alpha-adrenergic receptors greatly outnum-
ber them. The arterioles in skeletal muscle are an important
exception, however. Because they have a large number of beta-
2 adrenergic receptors, circulating epinephrine usually causes
vasodilation in this vascular bed.
Another hormone important for arteriolar control is
angiotensin II,
which constricts most arterioles. This peptide
is part of the renin-angiotensin system. Another important
hormone that causes arteriolar constriction is
vasopressin,
which is released into the blood by the posterior pituitary
gland (Chapter 11). The functions of vasopressin and angio-
tensin II will be described more fully in Chapter 14.
Finally, the hormone secreted by the cardiac atria—
atrial natriuretic peptide
—is a potent vasodilator. Whether
this hormone, whose actions on the kidneys are described in
Chapter 14, plays a widespread physiologic role in the control
of arterioles is unsettled.
Endothelial Cells and Vascular Smooth Muscle
It should be clear from the previous sections that many sub-
stances can induce the contraction or relaxation of vascu-
lar smooth muscle. Many of these substances do so by acting
directly on the arteriolar smooth muscle, but others act indi-
rectly via the endothelial cells adjacent to the smooth muscle.
Endothelial cells, in response to these latter substances as well as
certain mechanical stimuli, secrete several paracrine agents that
diffuse to the adjacent vascular smooth muscle and induce either
relaxation or contraction, resulting in vasodilation or vasocon-
striction, respectively.
One very important paracrine vasodilator released by
endothelial cells is nitric oxide; note that we are dealing here
with nitric oxide released from endothelial cells, not from
nerve endings, as described earlier. (Before the identity of the
vasodilator paracrine agent released by the endothelium was
determined to be nitric oxide, it was called
endothelium-
derived relaxing factor (EDRF),
and this name is still often
used because substances other than nitric oxide may also fi t
this general defi nition.) Nitric oxide is released continuously
in signifi cant amounts by endothelial cells in the arterioles and
contributes to arteriolar vasodilation in the basal state. In addi-
tion, its secretion rapidly and markedly increases in response
to a large number of the chemical mediators involved in both
refl ex and local control of arterioles. For example, nitric oxide
release is stimulated by bradykinin and histamine, substances
produced locally during infl
ammation (Chapter 18).
Another vasodilator the endothelial cells release is the
eicosanoid
prostacyclin (PGI
2
).
Unlike the case for nitric
Smooth muscle in skeletal muscle arterioles
Altered arteriolar radius
β
α
Plasma epinephrine
Norepinephrine in extracellular fluid
Sympathetic postganglionic
neurons to skeletal muscle arterioles
Release norepinephrine
Adrenal medulla
Secretes epinephrine
into blood
(Causes
vasoconstriction)
(Causes
vasodilation)
2
Figure 12–35
Effects of sympathetic nerves and plasma epinephrine on the
arterioles in skeletal muscle. After its release from neuron terminals,
norepinephrine diffuses to the arterioles, whereas epinephrine, a
hormone, is blood-borne. Note that activation of alpha-adrenergic
receptors and beta-2 adrenergic receptors produces opposing effects.
For simplicity, norepinephrine is shown binding only to alpha-
adrenergic receptors; it can also bind to beta-2 adrenergic receptors
on the arterioles, but this occurs to a lesser extent.
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