Neurohumoral vasoconstrictor systems in heart failure

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Abstract
By means of specific inhibitors of the renin–angiotensin system (captopril) and of the sympathetic nervous activity (prazosin) in dogs with congestive heart failure, and by using a specific antagonist of the pressor activity of arginine vasopressin in rats with heart failure, we studied the influence of these pressor hormone systems on peripheral vascular resistance and cardiac function. All three humoral vasoconstrictor systems were stimulated in heart failure. The experiments in dogs showed that the renin–angiotensin system plays an important role in the pathogenesis of heart failure by increasing peripheral vascular tone, thus impairing cardiac function, a mechanism which could be nearly completely prevented by converting enzyme inhibition. The increased sympathetic nervous activity was only insignificantly attenuated by the converting enzyme inhibition and its contribution tothe increase of peripheral vascular resistance was only small and transient. The rats with heart failure showed no effect of the vasopressin inhibitor on peripheral vascular resistance and cardiac function, despite plasma vasopressin levels which were 4 to 5 times higher than those in control animals. The inappropriately high secretion of vasopressin in relation to a decreased plasma osmolality may have contributed to the formation of edema and to the development of ‘dilutional hypoosmolality’.