Modulation of renal blood flow by endogenous endothelin-1 in conscious rabbits with left ventricular dysfunction

The current study addresses the functional status and role of the endothelin ETA receptor for renal vascular function in rabbits with and without heart failure (epinephrine-induced cardiomyopathy). Under baseline conditions, the ETA receptor antagonist BQ-123 did not change basal renal hemodynamics, but completely prevented endothelin-1 (ET-1)–induced renal vasoconstriction. In heart failure, in the presence of elevated plasma ET-1 concentrations (P< .05), renal vasoconstriction in response to exogenous ET-1 was intact. Unlike under baseline conditions, ETA receptor antagonism markedly increased renal blood flow (P<.05) and decreased renal vascular resistance (P< .05) in heart failure. The current study provides new insight into the pathophysiology of renal vasoconstriction associated with heart failure and the specific role of the renal ETA receptor in this pathophysiologic adaptation.