| Summary: | This study was designed to clarify the α1-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 α1A- and α1D-adrenoceptor antagonist, in a concentration-related manner. Neither BMY 7378 (100 nM), a selective α1D-adrenoceptor antagonist, nor chloroethylclonidine (60 µM), an α1B- and α1D-adrenoceptor antagonist, affected the tyramine-induced response. The results indicate that the noradrenaline released by tyramine may diffuse to the extrajunctional cleft, and thus it activates the extrajunctional α1A-adrenoceptors, because nerve stimulation-evoked second peaked vasoconstrictions were markedly inhibited by chloroethylclonidine but not by WB 4101. Keywords:: α1A-adrenoceptor, tyramine, splenic artery, canine, vascular neuroeffector transmission
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