Key result
Vasopressin blockade yields only modest hemodynamic reductions compared with teprotide in heart failure.
Why the study?
The renin-angiotensin system, sympathetic nerve activity, and vasopressin are all implicated in neurohumoral vasoconstriction in heart failure, motivating an investigation into the specific vasoconstrictive action of vasopressin.
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Minimal hemodynamic effect of vasopressin blockade versus teprotide in animal HF; leaves open its therapeutic role in humans.
Neurohumoral vasoconstrictor systems are activated in heart failure and influence left ventricular function by modifying pre- and afterload. The renin-angiotensin system, sympathetic nerve activity and vasopressin have all been implicated as mechanisms of vasoconstriction. We investigated the vasoconstrictive action of vasopressin by blocking its vascular receptors by a specific antagonist in animal models of heart failure due to rapid right ventricular pacing in dogs and to aortocaval fistula, pulmonary stenosis and aortic stenosis in rats. In all animal models studied, we observed an inappropirately elevated secretion of vasopressin in association with a decreased plasma osmolality. We found only a small reduction of aortic pressure and peripheral vascular resistance following the vasopressin inhibitor. The renin-angiotensin system and sympathetic nerve activity were activated in all animal models. We injected teprotide in order to test the role of angiotensin in the regulation of peripheral vascular tone, and found a much greater decrease of blood pressure and peripheral vascular resistance than caused by the vasopressin antagonist. These experiments suggest that vasopressin and the renin system increase peripheral vascular tone in certain models of heart failure, and demonstrate a much greater importance for the renin system.
A. J. G. Riegger (1988) studied Experimental heart failure. Specific vasopressin vascular receptor antagonist vs. Teprotide (angiotensin-converting enzyme inhibitor) was evaluated on Aortic blood pressure and peripheral vascular resistance. Vasopressin receptor blockade produced only a small reduction in aortic pressure and peripheral vascular resistance compared with a much greater decrease caused by teprotide in animal heart failure.