FUNCTIONAL 5-HT RECEPTOR SUBTYPES IN THE ISOLATED CANINE COMMON CAROTID-ARTERY

The vascular responses to 5-hydroxytryptamine (5-HT), 5-carboxamidotry ptamine (5-CT, a selective 5-HT1-like receptor agonist), alpha-methyl- 5-HT (alpha-M-5-HT, a relatively selective 5-HT2 receptor agonist), no radrenaline (NA), and KCl were examined in isolated, cannulated, and p erfused canine common carotid arterial preparations. They caused stron g vasoconstrictions. The rank order of vasoconstrictive potency was 5- HT > alpha-M-5-HT greater-than-or-equal-to NA > 5-CT much-greater-than KCl. The 5-HT-induced vasoconstriction was significantly depressed by methysergide (a 5-HT1 and 5-HT2 receptor antagonist), ketanserin (a s elective 5-HT2 receptor antagonist), and spiperone (a selective 5-HT2 receptor antagonist). The 5-CT- and alpha-M-5-HT-induced vasoconstrict ions were also significantly inhibited by methysergide, spiperone, and ketanserin. The NA-induced vasoconstriction was readily inhibited by bunazosin (an alpha-adrenoceptor antagonist) and ketanserin but not si gnificantly inhibited by spiperone and methysergide. KCl has a weak po tency for producing a vasoconstriction of the canine common carotid ar tery. A relatively large dose of diltiazem (a calcium channel blocker) did not modify 5-HT-induced vasoconstrictions. From these results, we conclude that (a) the canine common carotid artery contains abundant 5-HT receptors; (b) there are no functional 5-HT1 receptors, but 5-HT2 receptors are prominent; (c) 5-CT-induced vasoconstrictions might be due to activation of 5-HT2 but not to 5-HT1 receptors; (d) 5-HT-induce d vasoconstriction might not involve alpha-adrenoceptors; and (e) the vasoconstriction related to 5-HT in the common carotid artery is not s ignificantly mediated via activation of calcium ion channels of smooth muscle cells, but may be induced by calcium ions from intracellular s tores.