Ganong's Review of Medical Physiology, 23rd Edition

556
SECTION VI
Cardiovascular Physiology

resultant decrease in venous capacity increases venous return,
shifting blood to the arterial side of the circulation.

INNERVATION OF THE BLOOD VESSELS

Sympathetic noradrenergic fibers end on blood vessels in all
parts of the body to mediate vasoconstriction. In addition to
their vasoconstrictor innervation, resistance vessels in skeletal
muscles are innervated by vasodilator fibers, which, although
they travel with the sympathetic nerves, are cholinergic
(sym-
pathetic cholinergic vasodilator system).
There is no tonic ac-
tivity in the vasodilator fibers, but the vasoconstrictor fibers to
most vascular beds have some tonic activity. When the sympa-
thetic nerves are cut
(sympathectomy),
the blood vessels di-
late. In most tissues, vasodilation is produced by decreasing the
rate of tonic discharge in the vasoconstrictor nerves, although
in skeletal muscles it can also be produced by activating the
sympathetic cholinergic vasodilator system (Table 33–1).

CARDIAC INNERVATION

Impulses in the sympathetic nerves to the heart increase the
cardiac rate
(chronotropic effect),
rate of transmission in the
cardiac conductive tissue
(dromotropic effect),
and the force
of contraction
(inotropic effect).
They also inhibit the effects
of vagal parasympathetic stimulation, probably by release of
neuropeptide Y, which is a cotransmitter in the sympathetic
endings. Impulses in vagal fibers decrease heart rate. A mod-
erate amount of tonic discharge takes place in the cardiac sym-
pathetic nerves at rest, but there is a good deal of tonic vagal
discharge
(vagal tone)
in humans and other large animals. Af-
ter the administration of parasympatholytic drugs such as at-
ropine, the heart rate in humans increases from 70, its normal
resting value, to 150 to 180 beats/min because the sympathetic
tone is unopposed. In humans in whom both noradrenergic
and cholinergic systems are blocked, the heart rate is approxi-
mately 100 beats/min.

CARDIOVASCULAR CONTROL

The cardiovascular system is under neural influences coming
from several parts of the brain (see Figure 17–6), which in turn
receive feedback from sensory receptors in the vasculature (eg,
baroreceptors). A simplified model of the feedback control
circuit is shown in Figure 33–1. An increase in neural output
from the brain stem to sympathetic nerves leads to a decrease
in blood vessel diameter (arteriolar constriction) and increas-
es in stroke volume and heart rate, which contribute to a rise
in blood pressure. This in turn causes an increase in barore-
ceptor activity, which signals the brain stem to reduce the neu-
ral output to sympathetic nerves.
Venoconstriction and a decrease in the stores of blood in
the venous reservoirs usually accompany increases in arteri-
olar constriction, although changes in the capacitance vessels

do not always parallel changes in the resistance vessels. In the

presence of an increase in sympathetic nerve activity to the

heart and vasculature, there is usually an associated decrease

in the activity of vagal fibers to the heart. Conversely, a

decrease in sympathetic activity causes vasodilation, a fall in

blood pressure, and an increase in the storage of blood in the

venous reservoirs. There is usually a concomitant decrease in

heart rate, but this is mostly due to stimulation of the vagal

innervation of the heart.

MEDULLARY CONTROL OF

THE CARDIOVASCULAR SYSTEM

One of the major sources of excitatory input to sympathetic

nerves controlling the vasculature is neurons located near the

pial surface of the medulla in the rostral ventrolateral medulla

TABLE 33–1

Summary of factors affecting the caliber

of the arterioles.

Constriction Dilation

Local factors

Decreased local temperature Increased CO

2

and decreased O

2

Autoregulation Increased K

+

, adenosine, lactate, etc

Decreased local pH

Increased local temperature

Endothelial products

Endothelin-1 NO

Locally released platelet

serotonin

Kinins

Thromboxane A

2

Prostacyclin

Circulating hormones

Epinephrine (except in skele-

tal muscle and liver)

Epinephrine in skeletal muscle and

liver

Norepinephrine CGRP

α

AVP Substance P

Angiotensin II Histamine

Circulating Na

+

-K

+

ATPase

inhibitor

ANP

Neuropeptide Y VIP

Neural factors

Increased discharge of

sympathetic nerves

Decreased discharge of sympathetic

nerves

Activation of sympathetic cholinergic

vasodilator nerves to skeletal muscle