Dissociation of renin and aldosterone during low-dose epinephrine infusion

Besides its dose-dependent alpha- and beta-adrenoceptor-mediated vascular action, hormonal effects of epinephrine also involve the activation of renin secretion by direct stimulation of renal beta 1-adrenoceptors. To determine the interrelation between increased plasma renin activity in response to epinephrine and plasma aldosterone concentration and renal excretion of potassium and sodium, 26 normal subjects were subjected to 4 h of an intravenous infusion of low-dose epinephrine (12 ng/kg/min). Epinephrine infusion raised mean plasma epinephrine concentration 2.8-fold above control (P < .001). Plasma renin activity (PRA) increased by 56% (P < .01) during epinephrine infusion, whereas plasma aldosterone concentration remained constant. Infusion of epinephrine also resulted in markedly suppressed urinary potassium excretion (-32%; P < .025), while urinary sodium excretion was not altered. Serum potassium was decreased by 4.1% during epinephrine (P < .025). Systolic blood pressure and heart rate did not change, and diastolic blood pressure was slightly reduced by 5 mm Hg (P < .025). In summary, during low-dose epinephrine infusion PRA is markedly increased while plasma aldosterone remains unchanged. The fall in urinary potassium excretion in the presence of reduced serum potassium concentration is most likely mediated via the beta-adrenoceptor-mediated shift of potassium into cells. This in turn may prevent a concomitant rise of plasma aldosterone, which subsequently contributes to the blunted kaliuresis and unchanged natriuresis found during the epinephrine-induced rise of PRA. In conclusion, the epinephrine-induced fall in serum potassium appears to be the predominant regulator of plasma aldosterone concentration even in the presence of a stimulated PRA.