Beta-adrenergic-mediated extrarenal potassium disposal in patients with end-stage renal disease: Effect of propranolol

This study was designed to investigate beta-adrenergic-mediated extrarenal potassium disposal in patients with end-stage renal disease (ESRD). Plasma potassium was measured over a period of 3 months in 20 patients with ESRD who were receiving the nonselective beta-blocker propranolol (n=10) or not (n=10). Both groups were virtually anuric and had a comparable plasma BUN, plasma bicarbonate, and red cell Na-K-ATPase activity. Plasma potassium measured before dialysis was higher in propranolol users than in nonusers (5.6±0.2 and 4.6±0.1 mEq/l, p<0.005). To examine beta-adrenergic-mediated internal potassium disposal more directly, epinephrine and epinephrine plus propranolol were acutely administered to another group of patients with ESRD and to normal subjects. Epinephrine resulted in a similar fall in plasma potassium in both groups (0.69±0.20 and 0.63±0.07 mEq/l, respectively), thereby suggesting unimpaired beta-adrenergic-mediated extrarenal potassium handling in patients with ESRD. In patients, however, the response to epinephrine was heterogeneous. In 4 of the 10 patients studied, epinephrine infusion did not result in a decrement in plasma potassium suggesting impaired beta-adrenergic responsiveness and thus blunting of this mechanism of extrarenal potassium disposal. In the remaining 6 patients, epinephrine infusion resulted in a fall in plasma potassium which was greater than that observed in normal subjects (1.13±0.14 and 0.63±0.07 mEq/l, respectively, p<0.01). In the presence of propranolol, the infusion of epinephrine did not result in a decrement in plasma potassium in these 6 patients or in the 6 normal subjects (0.04±0.07 and -0.02±0.06 mEq/l, respectively). Our findings therefore indicate that in some patients with ESRD beta-adrenergic-mediated extrarenal potassium disposal is intact and thereby inhibitable by propranolol. Thus, the administration of propranolol to patients with ESRD is apt to precipitate hyperkalemia by obliterating beta-adrenergic-mediated extrarenal potassium disposal.