Page 360 - Anatomy and Physiology of Farm Animals, 8th Edition

Physiology of the Heart and Circulation / 345

This chapter discusses only some of the This tends to reduce blood volume and
therefore cardiac filling, cardiac output,
major regulators of arterial blood pressure
VetBooks.ir and blood volume and for didactic pur­ and blood pressure. Reductions in atrial
filling bring about increases in sympathetic
poses will classify these as neural reflexes,
circulating (humoral) agents, and parac­ nerve activity to the kidneys. This reflex
rine (locally produced) agents. Such also affects the secretion of renin from the
classifications require generalizations, kidneys (discussed later).
and there are many subtle interactions
among these classes that will not be Humoral Agents
explored in this text.

Renin is an enzyme released from the kid­
Neural Reflexes neys, and its release is regulated in part by
sympathetic nerve activity to the kidneys
and arterial blood pressure in the vessels
The arterial baroreceptor reflexes are perfusing the kidneys. Increases in renal
the neural reflexes primarily responsible sympathetic nerve activity and/or reduc­
for the short‐term or immediate regulation tions in arterial blood pressure to the
of arterial blood pressure. Neural receptors kidneys elicit increases in renin secretion
in the aorta and carotid arteries respond to (Fig. 18‐11). Renin acts on a plasma pro­
changes in arterial pressure in these vessels, tein substrate to produce a peptide, angio­
and this information is relayed to reflex tensin I, which an enzyme converts to
centers in the brainstem. The efferent angiotensin II. Angiotensin II constricts
nerves for these reflexes are the autonomic vascular smooth muscle, so it tends to
nerves to the heart and the sympathetic increase TPR and arterial blood pressure.
vasoconstrictor nerves to both arterioles Angiotensin II also reduces the urinary
and veins. Decreases in arterial blood pres­ loss of sodium chloride and water by its
sure bring about adjustments in these
efferent nerves to increase heart rate,
increase cardiac contractility, and promote Hypovolemia
arteriolar vasoconstriction and venocon­ Hypotension
striction. The overall effect tends to
increase both CO and TPR so that blood Renal perfusion pressure
pressure can be restored to its original
level. Increases in arterial blood pressure Renin secretion
above some original level should elicit
reductions in cardiac activity and relaxa­ Angiotensinogen Angiotensin I
tion of the vessels. Inhibition of vasocon­ Converting enzyme
strictor and venoconstrictor nerves is the
mechanism by which the reflex permits Angiotensin II
relaxation of the vascular smooth muscle.
Neural receptors in the atria of the heart Aldosterone
respond to changes in the volume of blood secretion Systemic
filling the atria, and afferent information blood pressure
from these receptors is relayed to brain­ Renal Na +
stem reflex centers. The primary efferents absorption
involved in these reflexes are the sympa­
thetic nerves to the kidneys. Increases in Extracellular Renin release
atrial filling bring about reductions in sym­ volume expansion
pathetic nerve stimulation of the kidneys, Figure 18-11. Renin‐angiotensin‐aldosterone
and this permits an increase in the urinary system response to hypovolemia and hypoten­
excretion of sodium chloride and water. sion. Source: adapted from Reece, 2015.