AJP - Regulatory, Integrative and Comparative Physiology, Vol 252, Issue 4 668-R673, Copyright © 1987 by American Physiological Society
Does vasopressin-induced vasoconstriction persist during prolonged infusion in dogs?
J. F. Liard
I have examined the systemic and regional hemodynamic effects of an
intravenous arginine vasopressin (AVP) infusion at a rate of 220 pg X kg-1
X min-1 maintained for 48 h in 12 conscious dogs. Plasma AVP concentration
increased from 2.8 +/- 1.1 to 8.2 +/- 1.4 pg/ml, and plasma osmolality fell
from 294.8 +/- 1.4 to 287.1 +/- 1.5 mosmol/kg. Mean arterial pressure
increased slightly but significantly despite a reduction in blood volume.
Contrary to what we previously observed with 1-h AVP infusion at the same
rate, cardiac output and heart rate did not decrease, and total peripheral
resistance did not increase. Most vascular beds sensitive to the acute
vasoconstrictor effects of AVP, such as those of the skeletal muscle, fat,
colon, and skin, did not show any significant reduction in blood flow after
48 h. Only in the pancreas and in the thyroid gland was there a significant
flow decrease, which was similar in magnitude to that measured after 1 h of
infusion. It therefore appears that vasoconstriction induced by modest
increases in plasma concentrations of AVP is not maintained during
prolonged administration in most vascular beds. However, injection of a
specific antagonist of the pressor action of AVP
[1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),
2-(O-methyl)tyrosine]arginine vasopressin, 10 micrograms/kg, induced a
significant increase in cardiac output and heart rate, as well as a fall in
total peripheral resistance and significant increases in myocardial, fat,
and skin blood flows after 48 h of AVP infusion.(ABSTRACT TRUNCATED AT 250
WORDS)
