CHAPTER 6 • NEUROHUMORAL CONTROL OF THE HEART AND CIRCULATION
129
and arterial blood pressure falls. Baroreceptor
reflexes (discussed later in this chapter) cause
the RVLM to increase sympathetic outflow to
stimulate the heart (increase heart rate and
inotropy) and to constrict the systemic vascu-
lature. These cardiac and vascular responses
help to restore normal arterial pressure. As
sympathetic neurons in the RVLM are being
activated, parasympathetic vagal activity orig-
inating from the DVN and nucleus ambiguus
is decreased. This is important because with-
out removal of vagal influences on the heart,
the ability of enhanced sympathetic activity
to increase heart rate is impaired. The reason
for this is that
vagal influences are dominant over
sympathetic influences in the heart.
Regions within the hypothalamus can inte-
grate and coordinate cardiovascular responses
by providing input to medullary centers. Stud-
ies have shown that electrical stimulation of
dorsomedial
hypothalamus
produces
auto-
nomic responses that mimic those that occur
during exercise, or the flight-or-fight response.
These coordinated responses include sympa-
thetic-mediated tachycardia, increased inotropy,
catecholamine release, and systemic vasocon-
striction. These are brought about by hypotha-
lamic activation of sympathetic neurons within
the RVLM and inhibition of vagal nuclei.
Input from higher cortical regions can
alter autonomic function as well. For exam-
ple, sudden fear or emotion can sometimes
cause vagal activation leading to bradycardia,
withdrawal of sympathetic vascular tone, and
fainting (vasovagal syncope). Fear and anxi-
ety can lead to sympathetic activation that
causes tachycardia, increased inotropy, and
hypertension.
Chronic sympathetic
activa-
tion induced by long-term emotional stress
can result in sustained hypertension, cardiac
hypertrophy, and arrhythmias.
CARDIAC AND VASCULAR AUTONOMIC
RECEPTORS
Activation of sympathetic efferent nerves to the
heart releases the neuro transmitter norepineph-
rine that binds primarily to P1-adrenoceptors
located in nodal tissue, conducting tissues,
and myocardium (see Fig. 6.4). There are also
postjunctional P2-adrenoceptors in the heart;
Heart
■ FIGURE 6.4 Adrenergic and muscarinic recep-
tors in the heart. Norepinephrine (NE) released
from sym pathetic nerve terminals binds to
postjunctional adrenoceptors (order of functional
importance: 31
> 32 > a1) to increase (+) inotropy,
chronotropy, and drom otropy. Prejunctional
a2-adrenoceptors serve as a feedback mechanism
to inhibit NE release. Parasympathetic (vagal)
nerves release acetylcholine (ACh), which binds to
postjunctional M2 receptors to decrease ( -) inot-
ropy, chronotropy, and drom otropy. ACh also binds
to prejunctional muscarinic receptors (M2) on
sym pathetic nerve terminals to inhibit NE release.
however, they are normally less important than
P1-adrenoceptors. Beta-adrenoceptors are cou-
pled to the Gs-protein/cAMP signal transduc-
tion pathway as described in Chapter 3. There
are
also
postjunctional
a 1-adrenoceptors
located in cardiac tissue that bind to norepi-
nephrine, which activates the Gq-protein/IP3
pathway to stimulate the heart (see Chapter 3).
Released norepinephrine can also bind to pre-
junctional a 2-adrenoceptors located on the
sympathetic nerve terminal. These receptors
inhibit norepinephrine release through a nega-
tive feedback mechanism.
Activation of postganglionic vagal fibers
causes the release of the neurotransmitter
ACh. In the heart, this neurotransmitter binds
to
muscarinic
receptors
(M2)
principally
in nodal tissue, and in atrial myocardium
(Fig. 6.4). These receptors are coupled to the
Gi-protein/cAMP signal transduction pathway
(see Chapter 3), which decreases chronotropy,
dromotropy, and inotropy (more so in the atria
than in the ventricles). Released ACh can also
bind to prejunctional M2 muscarinic receptors
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