THE ROLE OF ENDOGENOUS NOREPINEPHRINE RELEASE IN POTASSIUM-EVOKED VASOCONSTRICTION OF THE RAT TAIL ARTERY

Potassium-containing solutions are often used to study the sequence of events leading from excitation to vasoconstriction. In densely innervated vessels, such as the rat tail artery, potassium-induced vasoconstriction may be mediated via smooth muscle depolarization and release of endogeneous norepinephrine. The relative contribution of these two mechanisms - a 'direct' depolarization of the vascular smooth muscle cell membrane, and an 'indirect' sympathomimetic action - to the vasoconstrictor response was studied in the present paper. Perfusion/superfusion of the rat tail artery in vitro with potassium-containing solutions had different effects depending on the concentration used. A change in potassium concentration from 4.7 to 20 mM had no effect on either perfusion pressure or norepinephrine overflow. From 30 to 70 mM, potassium produced increasing amounts of norepinephrine overflow. Experiments with phentolamine and reserpine showed that this norepinephrine overflow contributed for up to half of the vasoconstrictor response observed. A second norepinephrine-independent mechanism was also involved but the latter appeared to be incapable of producing sustained contraction. At concentrations of potassium above 50-70 mM, the results of experiments with (+/-)-propranolol suggest that the norepinephrine released by potassium has a beta-adrenoceptor-mediated vasorelaxant effect.