Role of vasopressin in experimental congestive cardiac failure.
The hemodynamic and hormonal changes produced by adriamycin-induced cardiomyopathic congestive heart failure in rabbits were studied. Adriamycin cardiomyopathy in rabbits led to ventricular dilatation, pleural and pericardial effusions, hepatic congestion, and ascites. These pathological changes were associated with the maintenance of a normal blood pressure but a lowered cardiac output and increased total peripheral resistance. Plasma renin activity and plasma norepinephrine were increased twofold in rabbits with congestive cardiac failure. However, plasma vasopressin and osmolality were normal, whereas an increased vascular sensitivity to the infusion of exogenous vasopressin was demonstrated. Despite the normal levels of plasma vasopressin, administration of a specific vascular vasopressin antagonist led to a fall in blood pressure, a significant increase in cardiac output, and a decrease in total peripheral resistance. No such hemodynamic changes occurred on infusing normal rabbits with the vascular vasopressin antagonist, nor did any significant hemodynamic changes occur on injecting vehicle in rabbits with heart failure. These results suggest that in adriamycin-induced cardiomyopathic heart failure in rabbits, there is activation of the renin-angiotensin system and the sympathetic nervous system together with an increased sensitivity to vasopressin. These three hormonal systems help to maintain blood pressure by increasing total peripheral resistance in this experimental model of heart failure.
D000818:Animals; D004317:Doxorubicin; D005260:Female; D006333:Heart Failure / Q000139:chemically induced / Q000503:physiopathology*; D006728:Hormones / Q000097:blood; D007262:Infusions, Intravenous; D008297:Male; D011817:Rabbits; D014655:Vascular Resistance / Q000187:drug effects; D014667:Vasopressins / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000494:pharmacology*
D006728:Hormones; D014667:Vasopressins; D004317:Doxorubicin