PSIO 532 Study Guide - Midterm Guide: Group C Nerve Fiber, Adrenal Gland, Vagus Nerve
PSL – Cardiovascular System
ANP & C-fibers
In the atria walls, there are cells, which contain Atrial Natriuretic Peptide (ANP). As the walls
are stretched, ANP is released. ANP affects the kidney to decrease blood volume. ANP causes
Na+ and H20 to be lost in urine. Ex. When you have too much blood volume, the atria stretches,
which in turn releases ANP, which acts on the kidney to cause diuresis and natriuresis to
decrease the blood volume and bring it back towards normal.
Ventricular receptors: Response pattern is in general similar to that of arterial baroreceptors
and they tend to reinforce the arterial baroreflex. However, in severe circumstances they may
induce a "vicious cycle". In the walls of the left ventricle, there are free nerve endings, sensory
afferents (unmyelinated – ventricular c-fibers). These c-fibers normally do not have any activity,
but when they become active, they can be very powerful.
C-fibers are active during profound stress on the heart such a myocardial infarction, ischemia,
acidosis or even distortion of the arterial wall. During a severe hemorrhage, when the preload is
very low, and the sympathetic activity is very high, you will have a strong contraction of the left
etrile, ut you’ll e pupig dry lo preload → this can lead to distortion of the arterial
wall, and hence the C-fibers are activated. During severe hemorrhage, high circulating
catacholamines (especially epinephrine) and high sympathetic activity to the left ventricle
combined with very low preload activates ventricular receptors (C fibers) whose afferents
travel in the vagus nerve (vagal afferents) → C-fibers essentially tells the vasomotor to TURN
OFF sympathetic activity and TURN ON PNS! HOWEVER, this is not what we want during
severe hemorrhages → hence it could lead to hemorrhagic shock! Basically, during a
hemorrhage situation, the SNS activity rises and rises and then suddely, it just drops… ad this
is when C-fibers become active. SNS shuts down everywhere except for the adrenal gland →
adrenal gland continues to have high activity of SNS and continues to fire epinephrine. Epi
binds to the Beta-II receptors and causes vasodilation → THIS IS ALSO NOT WHAT WE WANT
DURING HEMORRHAGE. This is all part of the decompensatory phase of hemorrhagic shock. In
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