5-HT1B receptors and α2A/2C-adrenoceptors mediate external carotid vasoconstriction to dihydroergotamine

Dihydroergotamine produces external carotid vasoconstriction in vagosympathectomized dogs by 5-HT1B/1D receptors and α 2-adrenoceptors. This study identified the specific subtypes involved in this response. One-minute intracarotid infusions of dihydroergotamine (5.6-10 μg/min) dose-dependently decreased external carotid blood flow without affecting blood pressure or heart rate. This response was: (1) partly blocked in dogs pretreated intravenously with the antagonists SB224289 (5-HT1B; 2,3,6,7-tetrahydro-1′-methyl-5- [2′-methyl-4′ (5-methyl-1,2,4-oxadiazol-3-yl)biphenyl-4-carbonyl] furo[2,3-f]indole-3-spiro-4′-piperidine hydrochloride), rauwolscine (α2), BRL44408 (α2A; 2-[2H-(1-methyl-1,3- dihydroisoindole)methyl]-4,5-dihydroimidazole) or MK912 (α2C; (2S,12bS)-1′3′-dimethylspiro(1,3,4,5′,6,6′,7, 12b-octahydro-2Hbenzo[b]furo[2,3-a]quinazoline)-2,4′-pyrimidin-2′- one); (2) markedly blocked after SB224289 plus rauwolscine; and (3) unaffected after BRL15572 (5-HT1D; 1-(3-chlorophenyl)-4-[3,3-diphenyl (2-(S,R) hydroxypropanyl) piperazine] hydrochloride) or imiloxan (α2B). Therefore, the above response involves 5-HT1B receptors and α2A/2C-adrenoceptors.

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