Simulation of Spontaneous Secondary Hyperaldosteronism by Intravenous Infusion of Angiotensin II in Dogs with an Arteriovenous Fistula*

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Abstract
Dogs with a large arteriovenous fistula do not escape from the sodium-retaining effect of desoxycorticosterone or aldosterone; these animals were therefore employed to study the effects of angiotensin II in order that the octapeptide s actions which are mediated by aldosterone might be clearly evident. Dogs with a large arteriovenous fistula received a continuous intravenous infusion of angiotensin II for 6 to 11 days. Angiotensin produced complete sodium retention, edema formation, and lowered fecal sodium/potassium ratio but had little or no effect on arterial or venous pressures, potassium balance, or plasma sodium or potassium concentrations. Bilateral adrenalectomy prevented the sodium-retaining action of angiotensin when steroid replacement dosage was held constant. Hypersecretion of aldosterone occurred during angiotensin infusion in each of 2 dogs in which adrenocortical secretion rates were measured in the conscious state. Angiotensin II mimics the actions of desoxycorticosterone or aldosterone on urinary and fecal sodium excretion and on fecal potassium excretion, although the steroids tend to produce a decreased plasma potassium concentration in dogs with an a-v fistula. In the present experiments angiotensin produced the derangements of electrolyte metabolism that are characteristic of spontaneous secondary hyperaldosteronism.