Differences in alpha 1-adrenoceptor subtype-mediated vasoconstriction by tyramine and nerve stimulation in canine splenic artery.
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.
Yang
Xiao-Ping
XP
Department of Molecular Pharmacology, Shinshu University School of Medicine, Matsumoto 390-8621, Japan.
Chiba
Shigetoshi
S
D000320:Adrenergic Fibers / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation / Q000379:methods; D005260:Female; D008297:Male; D018340:Receptors, Adrenergic, alpha-1 / Q000145:classification / Q000502:physiology*; D013157:Splenic Artery / Q000187:drug effects* / Q000502:physiology; D014439:Tyramine / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
D018340:Receptors, Adrenergic, alpha-1; D014439:Tyramine