Abstract
Summary
Experiments were undertaken in dogs to determine the contribution of deoxycorticosterone (DOC) to the increased mineralocorticoid activity in heart failure. Chronic experimental heart failure occurred secondary to induced tricuspid insufficiency and pulmonic stenosis. Simultaneous measurements of DOC, corticosterone and aldosterone revealed average secretion rates of 0.18, 1.50, and 0.020 μg/min respectively for eight normal dogs and 0.18, 1.33, and 0.097 μg/min for five dogs with heart failure. The fivefold increase in aldosterone secretion was significant at the 5% level. Because of earlier evidence for increased activity of the renin-angiotensin system in experimental heart failure, the effect of angiotensin II on steroid secretion was studied. In acute experiments, intravenous infusion of angiotensin II in normal dogs increased DOC secretion. The explanation for the finding of a normal rate of DOC secretion in heart failure whereas acutely angiotensin II increased DOC secretion is not clear.
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