HYPERSECRETION OF ALDOSTERONE IN DOGS WITH A CHRONIC AORTIC-CAVAL FISTULA AND HIGH OUTPUT HEART FAILURE.

Abstract

Hypersecretion of aldosterone occurred at the onset of signs of congestive heart failure in a large series of dogs with a large infrarenal aortic-caval fistula. There was evidence of right heart failure in all animals and in four of the dogs râles or frank pulmonary edema was present. Marked sodium retention and ascites or edema were consistent findings and in the majority of the animals central venous pressure was elevated. Hypophysectomy was followed by a striking fall in both aldosterone and corticosterone secretion but in several animals hypersecretion of aldosterone was evident in the absence of the anterior pituitary. Subsequent acute bilateral nephrectomy of these hypophysectomized dogs resulted in a marked drop of aldosterone secretion to a very low level, and a precipitous fall in arterial pressure frequently occurred. An intravenous infusion of a saline extract of each animal's kidneys produced a striking elevation in aldosterone output; corticosterone secretion and arterial pressure increased consistently. The kidneys of these dogs with heart failure secondary to an A-V fistula frequently showed hypergranulation and hyperplasia of the juxtaglomerular cells. The present findings suggest that the increased rate of aldosterone secretion was mediated by the renin-angiotensin system. Measurements of arterial pressure and renal hemodynamic function demonstrated a fall of mean renal arterial pressure, glomerular filtration rate, and renal plasma flow, whereas arterial pulse pressure above the fistula and presumably in the kidneys was increased. The data suggest that decreased pulse pressure is unnecessary for activation of the renal mechanism leading to hyperaldosteronism.