AJP - Regulatory, Integrative and Comparative Physiology, Vol 251, Issue 3 525-R530, Copyright © 1986 by American Physiological Society
Pressor resistance to vasopressin in sodium depletion, potassium depletion, and cirrhosis
B. M. Murray and M. S. Paller
Resistance to the pressor effects of angiotensin II, but not
norepinephrine, has been observed in sodium depletion, potassium depletion,
and cirrhosis. We tested the response to arginine vasopressin (AVP) in each
of these conditions. Male Sprague-Dawley rats were made sodium depleted
with furosemide and a low-sodium diet for 3 days, potassium depleted by
feeding a low-potassium diet for 14-21 days, or cirrhotic by inhalation of
carbon tetrachloride for 8 wk. In conscious rats, the pressor response to
graded doses of AVP was reduced in sodium depletion by 27-43% compared with
control rats. Sodium-depleted rats were also found to have enhanced
baroreceptor reflexes, since the decrease in heart rate for a given
increase in mean arterial pressure was greater than in control rats. When
the ganglionic blocker pentolinium tartrate was given to sodium-depleted
rats the pressor response to AVP was restored to control levels. In
potassium-depleted rats the pressor response to AVP was 21-52% lower than
that in controls, whereas cirrhotic rats also had a blunted response to AVP
(14-41% lower than control). However, there was no evidence in either of
these two states of enhanced baroreceptor activity, and pretreatment with
pentolinium tartrate did not restore the pressor response to normal.
Therefore, although resistance to the pressor effect of AVP was found in
all three conditions, the mechanism of this effect was different in sodium
depletion compared with potassium depletion and cirrhosis. We conclude that
resistance to the pressor action of AVP in sodium depletion was secondary
to resetting of the baroreceptors.
