Plasma Renin Activity and the Effects of Deoxycorticosterone Acetate in Dogs with Chronic Left Ventricular Overload

Abstract

Chronic left ventricular overload and left heart failure were produced by an aortic-left atrial shunt and superimposed aortic constriction. With the shunt alone, plasma renin activity and sodium balance were normal. Superimposed aortic constriction produced a further elevation in left ventricular end diastolic pressure (LVEDP), increased plasma renin activity and sodium retention occurred. Seven dogs died in pulmonary edema within a week, but nine others recovered with a return in plasma renin activity and sodium excretion to normal. Five of these nine dogs that survived the acute effects of aortic stenosis developed pulmonary edema at least 7 days after aortic constriction; LVEDP was markedly elevated, plasma renin activity was high and sodium retention occurred. Six other dogs with chronic left ventricular overload, but not retaining sodium, were given deoxycorticosterone acetate (DOCA), 15 mg/day, to study the response in renal sodium excretion. In two of the dogs, LVEDP was below 35 mm Hg and the normal "escape" pattern, characterized by return of sodium excretion to the normal control level, was observed. However, in the other four animals, LVEDP was above 35 mm Hg, escape failed to occur and marked sodium retention resulted; a further elevation of LVEDP was observed and pulmonary edema occurred on four occasions. The failure of dogs with marked elevation of LVEDP to escape from DOCA indicates that other factors in addition to the renin-angiotensin-aldosterone system are involved in the sodium retention of left ventricular failure.