Antinatriuresis associated with propranolol administration in the dog.

Abstract

There is evidence to suggest that the sympatheticnervous system plays a role in the regulation of renal sodium excretion. In the present experiments, the pattern of renal sodium and water excretion following the intravenous infusion of pro pranolol (a β-adrenergic blocking agent) was studied by clearance techniques in nine normal dogs under hydropenic conditions undergoing a modest mannitol diuresis. Blood pressure and pulse rate were monitored throughout. Following systemic administration of propranolol there was a significant decrease in fractional sodium excretion of 2.0 ml/min/100 ml GFR. This occurred despite a 14.2-percent increase in glomerular filtration rate. Potassium excretion and solute-free water reabsorption decreased. There were no significant or predictable changes in heart rate, mean arterial blood pressure, effective renal plasma flow or filtration fraction. These data indicate that propranolol increases renal tubular sodium reabsorption in the dog and suggest that the site of action is in the proximal tubule. Moreover, the data suggest that the mechanism of action is not primarily related to alterations in systemic or renal hemodynamics but may be due to a direct effect on renal tubular sodium transport.