Differences in α1-Adrenoceptor Subtype-Mediated Vasoconstriction by Tyramine and Nerve Stimulation in Canine Splenic Artery

Abstract

Abstract. This study was designed to clarify the α 1 -adrenoceptor subtypes mediating the vasoconstrictor response to tyramine in isolated and perfused canine splenic artery. It was shown that tyramine potentiated the nerve stimulation-induced second peaked vasoconstriction that was readily suppressed by prazosin treatment. A bolus injection of tyramine (0.01 -0.3 µmol) caused a vasoconstriction in a dose-related manner. The tyramine-induced vasoconstriction was inhibited by WB 4101 (10 and 100 nM), an α 1A -and α 1D -adrenoceptor antagonist, in a concentrationrelated manner. Neither BMY 7378 (100 nM), a selective α 1D -adrenoceptor antagonist, nor chloroethylclonidine (60 µM), an α 1B -and α 1D -adrenoceptor antagonist, affected the tyramineinduced response. The results indicate that the noradrenaline released by tyramine may diffuse to the extrajunctional cleft, and thus it activates the extrajunctional α 1A -adrenoceptors, because nerve stimulation-evoked second peaked vasoconstrictions were markedly inhibited by chloroethylclonidine but not by WB 4101.