Propranolol induces acute natriuresis by β blockade and dopaminergic stimulation

Abstract

Dl-Propranolol (0.8–1.6 mg/kg∙h for 1 h) produced a transient two- to three-fold increase in sodium excretion in nondiuretic rats infused with Pitressin and aldosterone and in water diuretic rats. Sodium excretion increased more in rats depleted of renin by chronic Doca and salt administration than in rats maintained on a low salt diet. An angiotensin inhibitor (1,sarcosine-8,valine angiotensin II) decreased sodium excretion. Therefore the natriuresis was not mediated by antidiuretic hormone, aldosterone, or renin–angiotensin. d-Propranolol did not produce a natriuresis. Prior treatment with phenoxybenzamine did not prevent the natriuretic response but chlorisondamine pretreatment did. The natriuresis is produced by β blockade and requires postganglionic nerve function but is independent of α receptors. dl-Propranolol decreased heart rate and cardiac output but systemic pressure did not fall and renal blood flow increased. This suggests a dopamine-mediated renal vasodilation and natriuresis. Haloperidol and pimozide, both dopamine blocking agents with minimal β blocking effects, prevented the natriuretic response. We conclude that propranolol may increase sodium excretion directly by blocking β receptors in the distal nephron and indirectly by dopamine-mediated renal vasodilation.