1. Differences in alpha 1-adrenoceptor subtype-mediated vasoconstriction by tyramine and nerve stimulation in canine splenic artery.
- Author
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Yang XP and Chiba S
- Subjects
- Adrenergic Fibers drug effects, Animals, Dogs, Dose-Response Relationship, Drug, Electric Stimulation methods, Female, Male, Receptors, Adrenergic, alpha-1 classification, Splenic Artery physiology, Vasoconstriction drug effects, Adrenergic Fibers physiology, Receptors, Adrenergic, alpha-1 physiology, Splenic Artery drug effects, Tyramine pharmacology, Vasoconstriction physiology
- Abstract
This study was designed to clarify the alpha(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 micromol) caused a vasoconstriction in a dose-related manner. The tyramine-induced vasoconstriction was inhibited by WB 4101 (10 and 100 nM), an alpha(1A)-and alpha(1D)-adrenoceptor antagonist, in a concentration-related manner. Neither BMY 7378 (100 nM), a selective alpha(1D)-adrenoceptor antagonist, nor chloroethylclonidine (60 microM), an alpha(1B)- and alpha(1D)-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 alpha(1A)-adrenoceptors, because nerve stimulation-evoked second peaked vasoconstrictions were markedly inhibited by chloroethylclonidine but not by WB 4101.
- Published
- 2005
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