Page 361 - Anatomy and Physiology of Farm Animals, 8th Edition

346 / Anatomy and Physiology of Farm Animals

action on tubules in the kidney and by II and norepinephrine) are known to
stimulate endothelin release. Interestingly,
promoting the release of aldosterone from
VetBooks.ir the adrenal cortex. The overall biologic circulating vasoconstrictors tend to increase
the release of this locally produced
effect of angiotensin II is to increase arte­
rial pressure and blood volume. vasoconstrictor.
At rest, the plasma levels of epinephrine
and norepinephrine are relatively low, so
their effects on cardiac function and Cardiovascular Function During
vascular smooth muscle are relatively Exercise and Hypovolemia
minor. However, plasma levels can increase
significantly in highly stressed animals or in Increases in cardiac output and rate of
response to severe reductions in blood pres­ blood flow to skeletal muscle are needed
sure or blood volume. In these conditions, during exercise to meet the increased
circulating epinephrine and norepinephrine metabolic needs of the active skeletal
promote increases in cardiac function and muscle. Several of the cardiovascular
constrict vascular smooth muscle. adjustments during exercise are learned
Atrial natriuretic peptides (ANPs) are responses or behavior responses that
released from the atria of the heart in begin just prior to or at the initiation of
response to increases in blood volume and exercise. These are apparently initiated by
atrial filling. ANPs promote an increase in the cerebral cortex, involve autonomic
the urinary excretion of sodium and water nerves, and include an increased heart
by a direct action on tubules in the kidney. rate and vasodilation of arterioles supply­
ANPs also reduce TPR by relaxing arteri­ ing skeletal muscle. Increased circulating
olar vascular smooth muscle that was levels of epinephrine may also contribute
constricted by vasoconstrictor agents. to these changes. After exercise has begun,
appropriate vasodilation of arterioles sup­
Paracrine Agents plying active skeletal muscles is primarily
maintained by local metabolites produced
Endothelial cells lining many blood vessels by the active muscles. Typically, the
produce and release nitric oxide, a local increase in cardiac function is greater than
vasodilator. Nitric oxide release by the degree of vasodilation, so arterial pres­
endothelial cells is subject to regulation by sure rises slightly. Vascular resistance
a variety of agents, and the importance of increases in other organs whose metabo­
its overall role in the regulation of TPR in lism is not increased during exercise, and
normal animals is controversial. Bacterial this prevents an increased blood flow
endotoxins are lipopolysaccharide com- to these organs. During exercise, the
ponents of the bacterial cell wall that are increased cardiac output (increased heart
released when the cell is lysed. These rate and contractility) is maintained by
endotoxins stimulate macrophages sympathetic stimulation of the heart.
throughout an animal’s body to produce This sympathetic stimulation is primarily
and release unusually large amounts of maintained by the mechanisms originat­
nitric oxide. General overproduction of ing in the cerebral cortex and by reflexes
nitric oxide causes widespread vasodila- based on afferent information originating
tion and a severe drop in arterial blood in the exercising skeletal muscle.
pressure. These cardiovascular changes Hypovolemia is abnormally decreased
are part of a clinical syndrome, endo- circulating fluid volume (i.e., blood vol­
toxic or septic shock. ume). It can occur rapidly, as a result of
Endothelial cells also secrete a peptide, hemorrhage, or slowly, as a result of dehy­
endothelin, which constricts vascular dration. Reduced blood volume results in
smooth muscle of arterioles. As with nitric reduced cardiac filling pressure and ven­
oxide, a variety of agents (e.g., angiotensin tricular filling (i.e., reduced end‐diastolic