Increased 86Rb+ efflux from perfused rat hearts exposed to alpha 1-adrenergic stimulation.

Stimulation of myocardial alpha 1-adrenoceptors mediates changes in potassium fluxes across the sarcolemma. We studied the effect of alpha 1-adrenoceptor stimulation (5 x 10(-5) M phenylephrine with addition of 10(-6) M timolol) on potassium efflux by use of 86Rb+ efflux from isolated rat hearts perfused in a nonrecirculation system. The hearts were loaded with 86Rb+, followed by washout during which they were exposed to alpha 1-adrenergic stimulation with or without addition of the Na+/K(+)-ATPase inhibitor ouabain (10(-5) M). 86Rb+ content in perfusate fractions during the washout period and in the hearts at the end of experiments was measured; 86Rb+ efflux rates were determined as the ratio between the radioactivity of the perfusate fractions and the corresponding radioactivity contents of the hearts. alpha 1-adrenoceptor stimulation evoked a gradual increase in 86Rb+ efflux amounting to 30% of reference value after 20 min. With addition of ouabain, the alpha 1-adrenergic increase in 86Rb+ efflux developed faster and reached a maximum of approximately 40% of basal after approximately 10 min. The effects both with and without addition of ouabain were prevented by the alpha 1-adrenoceptor blocker prazosin (10(-6) M). Results indicate that increased potassium efflux is a part of alpha 1-adrenergic heart effects.