AJP - Heart and Circulatory Physiology, Vol 258, Issue 6 1882-H1888, Copyright © 1990 by American Physiological Society
Attenuation of pressor responses to arginine vasopressin in right-sided congestive heart failure
C. K. Stone, N. Imai, C. D. Sladek and C. S. Liang
Department of Medicine, University of Rochester Medical Center, New York 14642.
Although arginine vasopressin (AVP) is elevated in heart failure,
inhibition of the vasopressinergic V1-receptor produces minimal changes in
blood pressure. To determine whether the V1 vasoconstrictor effect is
attenuated in heart failure, we randomly administered three increasing
doses of AVP and methoxamine intravenously to 11 dogs with right-sided
congestive heart failure (RHF) and 7 sham-operated dogs. Plasma AVP was
elevated in RHF (21 +/- 3 pg/ml) compared with sham-operated dogs (3.8 +/-
0.6 pg/ml). While the pressor response to methoxamine was similar in the
two groups, AVP caused a smaller increase in mean aortic pressure in RHF
dogs than sham-operated dogs. To determine whether the difference in the
pressor response to AVP was caused by greater reflex withdrawal of the
sympathetic activity in RHF than sham-operated dogs, we also administered
AVP after these animals had been pretreated with prazosin and propranolol.
Adrenoceptor blockade exaggerated the pressor response to AVP; however, the
increase in mean aortic pressure was still smaller in RHF than
sham-operated dogs. The diminished pressor response in adrenoceptor-blocked
RHF dogs was associated with a smaller increase in total peripheral
vascular resistance compared with similarly treated sham dogs. Thus,
although the pressor response to AVP was offset by baroreflex activation,
the attenuated pressor effect of AVP in heart failure cannot be explained
by sympathetic withdrawal alone. AVP probably exerts a smaller direct
vasoconstrictor effect when the vasopressinergic system is chronically
activated in heart failure.
