Experimental study reveals that cardiac glycosides reduce aldosterone secretion during hemodynamic improvement in dogs with heart failure, indicating circulatory regulation of hormone production.
A marked elevation in the rate of aldosterone secretion was observed in eight dogs with experimental congestive heart failure secondary either to controlled progressive pulmonic stenosis or to combined tricuspid insufficiency and pulmonic stenosis, and in one dog with spontaneously occurring congestive heart failure. In the dogs with pulmonic stenosis, digitalization with digoxin resulted in improvement in cardiovascular function, and subsequent further constriction of the pulmonary artery again led to right ventricular failure; in each animal aldosterone output decreased within 90 minutes after digitalization, and increased markedly within one hour after further constriction of the pulmonary artery. In the dog with naturally occurring congestive heart failure, ouabain administration caused a similar striking hemodynamic improvement, and a marked reduction in aldosterone secretion was observed within 55 minutes after the glycoside was given. In the dogs with combined tricuspid insufficiency and pulmonic stenosis, no hemodynamic improvement occurred after digitalization; in these animals, the aldosterone secretion rate did not change significantly during the two-hour period following the digoxin injection. These data demonstrate that changes in the rate of aldosterone secretion in dogs with right heart failure were closely correlated with alterations in cardiovascular function; in these animals, hemodynamic improvement consistently led to decreased aldosterone production, and subsequent worsening of cardiovascular function resulted in increased aldosterone output.
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Carpenter et al. (1962) studied this question.
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