Abstract
The vascular responses of simian gastroepiploic arteries to 5-hydroxytryptamine (5-HT), 5-carboxamidotryptamine (5-CT, a selective 5-HT 1-like receptor agonist), 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, a selective 5-HT 1A receptor agonist), m-trifluoromethylphenylpiperazine (TFMPP, a selective 5-HT 1B receptor agonist), noradrenaline and KCl were examined in isolated, cannulated and perfused preparations. 5-HT induced dose-dependent vasoconstrictions more potently than noradrenaline did. The rank order of potency was 5-HT > noradrenaline > 5-CT > 8-OH-DPAT = TFMPP. 5-HT- and 5-CT-induced vasoconstrictions were not significantly changed by endothelial denutation, although acetylcholine-induced vasodilatations were abolished. 5-HT-induced vasoconstrictions were depressed by phentolamine (an α-adrenoceptor antagonist), diltiazem (a calcium ion channel inhibitor), methysergide (a 5HT 1- and 5HT 2-receptor antagonist) and ketanserin (a selective 5-HT 2 receptor antagonist). Noradrenaline-induced vasoconstrictions were readily inhibited by phentolamine and ketanserin. 5-CT-, 8-OH-DPAT- and TFMPP-induced vasoconstrictions were inhibited by both methysergide and ketanserin. KCl-induced vasoconstrictions were blocked by diltiazem. From these results, we concluded that (1) the simian gastroepiploic artery contains 5-HT receptors, (2) 5-HT 1-like and 5-HT 2 receptors are involved in the vasoconstriction of the simian gastroepiploic artery, and (3) the vasoconstriction is at least partially related to the activation of calcium ion channels.
Published Version
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