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Background Efficacy of diuretic therapy in congestive heart failure (CHF) can be affected by renal hemodynamics, neurohumoral activation, and diuretic-induced changes in renal function. Physiological strategies that enhance water and sodium (Na) excretion while maintaining renal function are a high priority. Arginine vasopressin increases water reabsorption after binding to the V2 receptor in the collecting duct (CD). In contrast, B-type natriuretic peptide (B) decreases Na reabsorption via the particulate guanylyl cyclase linked natriuretic peptide A receptor (NPR-A) also in the CD. We hypothesized that coadministration of the V2-receptor antagonist tolvaptan (T) and B would mediate a diuresis and natriuresis without adversely affecting renal hemodynamics in experimental CHF.

bmc pharmacology

Coadministration of B-type natriuretic peptide and the vasopressin-2 receptor antagonist tolvaptan: a novel physiologic strategy to enhance water and sodium excretion without adversely affecting renal or neurohumoral function in experimental congestive heart failure