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Impairment of extrarenal potassium disposal by alpha-adrenergic stimulation.

Since beta-adrenergic stimulation enhances extrarenal potassium uptake, we postulated an opposite effect of the alpha-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 alpha-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 less than 0.025) and prolonged it, without changing urinary potassium excretion. Subsequent administration of potassium and phenylephrine together with the alpha-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 alpha-adrenergic receptors impairs extrarenal disposal of an acute potassium load--the opposite effect of beta-adrenergic stimulation. The alpha-adrenergic effect may act to preserve a normal serum potassium level or may contribute to hyperkalemia under certain circumstances, such as vigorous exercise.