DISSOCIATION OF RENIN AND ALDOSTERONE DURING LOW-DOSE EPINEPHRINE INFUSION

Besides its dose-dependent alpha- and beta-adrenoceptor-mediated vascu lar action, hormonal effects of epinephrine also involve the activatio n of renin secretion by direct stimulation of renal beta(1)-adrenocept ors. To determine the interrelation between increased plasma renin act ivity in response to epinephrine and plasma aldosterone concentration and renal excretion of potassium and sodium, 26 normal subjects were s ubjected to 4 h of an intravenous infusion of low-dose epinephrine (12 ng/kg/min). Epinephrine infusion raised mean plasma epinephrine conce ntration 2.8-fold above control (P < .001). Plasma renin activity (PRA ) increased by 56% (P < .01) during epinephrine infusion, whereas plas ma aldosterone concentration remained constant. Infusion of epinephrin e also resulted in markedly suppressed urinary potassium excretion (-3 2%; P < .025), while urinary sodium excretion was not altered. Serum p otassium was decreased by 4.1% during epinephrine (P < .025). Systolic blood pressure and heart rate did not change, and diastolic blood pre ssure was slightly reduced by 5 mm Hg (P < .025). In summary, during l ow-dose epinephrine infusion PRA is markedly increased while plasma al dosterone remains unchanged. The fall in urinary potassium excretion i n the presence of reduced serum potassium concentration is most likely mediated via the beta-adrenoceptor-mediated shift of potassium into c ells. This in turn may prevent a concomitant rise of plasma aldosteron e, which subsequently contributes to the blunted kaliuresis and unchan ged natriuresis found during the epinephrine-induced rise of PRA. In c onclusion, 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.