130
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
found
on
nearby
sympathetic
adrenergic
nerve terminals, which inhibits their release
of norepinephrine.
In blood vessels, norepinephrine released
by sympathetic adrenergic nerves preferen-
tially binds to postjunctional a-adrenoceptors
to cause smooth muscle contraction and vaso-
constriction (see Fig. 6.5). Similar responses
occur when norepinephrine binds to postjunc-
tional a 2-adrenoreceptors located primarily
on small arteries and arterioles, although
postjunctional a —adrenoceptors are generally
the more important a-adrenoceptor subtype
in most vessels. These a-adrenoceptors are
coupled to the Gq-protein/IP3 signal trans-
duction pathway as described in Chapter 3.
In
addition,
norepinephrine
can
bind
to
prejunctional a 2-adrenoreceptors, which acts
as a negative feedback mechanism for modu-
lating norepinephrine release.
Blood
vessels
possess
postjunctional
P2-adrenoceptors in addition to a-adrenoceptors.
Activation of postjunctional P2-adrenoceptors by
norepinephrine (and, more importantly, by cir-
culating epinephrine) causes vasodilation in the
absence of opposing a-adrenoceptor-mediated
■ FIGURE 6.5 Adrenergic and muscarinic
receptors in blood vessels. Norepinephrine (NE)
released from sym pathetic nerve terminals
binds to postjunctional adrenoceptors (order of
functional importance: a, > a2 > ß2). NE binding to
postjunctional a-adrenoceptors causes increased
(+) vascular tone (vasoconstriction), whereas
binding to ß2-adrenoceptors causes decreased
( -) vascular tone (vasodilation). In a few specific
organs (e.g., genitalia), ACh released by parasym-
pathetic nerves binds to vascular M2 receptors to
produce endothelial-dependent vasodilation.
vasoconstriction. To observe this P2-adrenoceptor-
induced vasodilation experimentally, one can
stimulate vascular sympathetic nerves in the
presence of complete a-adrenoceptor blockade.
Normally, this small P2-receptor-mediated vaso-
dilator effect of norepinephrine is completely
overwhelmed by simultaneous a-adrenoceptor
activation, leading to vasoconstriction.
Although there is relatively little or no
parasympathetic innervation of most blood
vessels in the body, M2 muscarinic receptors
on coronary arteries can respond to vagal acti-
vation in the heart by dilating, and s imilar
receptors in genital erectile tissue respond by
dilating to ACh release by parasympathetic
nerves (Fig. 6.5).
Baroreceptor Feedback
Regulation of Arterial Pressure
As described above, sympathetic nerves play
an important role in regulating systemic vas-
cular resistance and cardiac function, and
therefore arterial blood pressure. But, how
does the body control the systemic vascular
resistance and cardiac output to establish and
maintain an arterial blood pressure to ensure
adequate organ perfusion?
Arterial blood pressure is regulated through
negative feedback systems incorporating pres-
sure sensors (i.e., baroreceptors) found in
strategic locations within the cardiovascular
system. Arterial baroreceptors are found in
the carotid sinus (at the bifurcation of external
and internal carotids) and in the aortic arch
(Fig. 6.6). The sinus nerve (nerve of Hering), a
branch of the glossopharyngeal nerve (cranial
nerve IX), innervates the carotid sinus. Affer-
ent fibers from the carotid sinus travel in the
glossopharyngeal nerve up to the brainstem,
where they synapse at the NTS. As already
described, the NTS modulates the activity of
sympathetic neurons within the RVLM and
medullary vagal nuclei. The aortic arch baro-
receptors are innervated by the aortic nerve,
which then combines with the vagus nerve
(cranial nerve X) before traveling to the NTS.
The arterial baroreceptors respond to the
stretching of the vessel walls produced by
increases in arterial blood pressure (Fig. 6.7).
Increased arterial pressure increases the firing
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