Impairment of Extrarenal Potassium Disposal by α-Adrenergic Stimulation

Since β-adrenergic stimulation enhances extrarenal potassium uptake, we postulated an opposite effect of the α-adrenergic nervous system. Seven healthy subjects were given intravenous potassium chloride (0.5 mmol per kilogram of body weight), in the presence and absence of the α-agonist phenylephrine. After potassium chloride alone, the potassium level rose to 0.64±0.03 mmol (mean ±S.E.M.); phenylephrine augmented the rise (0.93±0.09 mmol, P<0.025) and prolonged it, without changing urinary potassium excretion. Subsequent administration of potassium and phenylephrine together with the α-antagonist phentolamine blocked the rise in the potassium level due to phenylephrine and shortened the duration of elevation, again without affecting urinary potassium excretion. No changes in plasma renin and aldosterone levels or in serum insulin concentrations occurred, to account for these findings. Stimulation of α-adrenergic receptors impairs extrarenal disposal of an acute potassium load — the opposite effect of β-adrenergic stimulation. The α-adrenergic effect may act to preserve a normal serum potassium level or may contribute to hyperkalemia under certain circumstances, such as vigorous exercise. (N Engl J Med 1984; 311:145–9.).