Beta adrenergic control of extrarenal potassium disposal. A beta-2 mediated phenomenon.

Abstract

Beta adrenergic control of extrarenal potassium disposal was evaluated by examining the effects of physiologic doses of beta adrenergic agonists and antagonists on potassium tolerance in acutely nephrectomized rats. Following an acute intravenous potassium load (0.17 mEq/100 g over 60 min), the plasma potassium concentration rose significantly less in animals concomitantly treated with epinephrine at a dose that raises plasma epinephrine concentration to levels found during surgical stress (maximum plasma K 2.2 vs. 2.9 mEq/1 in controls receiving KCl alone; p less than 0.005). Similar results were observed with the selective beta-2 agonists salbutamol and terbutaline. Conversely, the rise in plasma potassium concentration was significantly greater in rats treated with low-dose propranolol (beta-1 + beta-2 blockade) and with butoxamine (beta-2 blockade) compared to control animals. In contrast, the selective beta-1 blocking agent metoprolol had no effect on potassium tolerance. Alterations in potassium tolerance following the administration of various beta adrenergic agonists and antagonists could not be explained by changes in plasma insulin, renin, or glucose concentration or by differences in the acid-base or hemodynamic status of the animals. The data suggest that beta adrenergic control of extrarenal potassium disposal occurs with physiologic stimulation or blockade of the beta-2 receptor site.