Ito T, Chiba S
J Pharmacol Exp Ther. 1985 Sep;234(3):698-702.
Four alpha adrenergic agonists (phenylephrine, xylazine, clonidine and norepinephrine) and two antagonists (prazosin and yohimbine) were used to investigate the characteristics of the postjunctional alpha adrenoceptors involved in contraction of the isolated and perfused canine intermediate auricular artery. All agonists showed almost equal potencies for inducing vasoconstriction in the perfused arterial preparations (i.e., all agonists caused strong vasoconstrictor responses in a dose-related manner; the threshold dose of each agonist was within a dose range of 0.003 to 0.01 micrograms and 0.3 to 1.0 micrograms of each agent caused approximately 200 mm Hg increase in perfusion pressure). Prazosin inhibited phenylephrine-induced vasoconstriction in a competitive manner, but yohimbine did not significantly influence phenylephrine-induced responses. Xylazine-induced responses were inhibited by both prazosin and yohimbine, but the former was less potent than the latter at a low dose and the antagonistic property of prazosin against xylazine was not competitive. The pA2 values of prazosin against phenylephrine, xylazine and clonidine were 7.10, 6.82 and 6.99, respectively, and that of yohimbine against xylazine was 7.16. These results support the theory that not only alpha-1 but also alpha-2 adrenoceptors are involved in the contractile responses of the isolated and perfused canine intermediate auricular artery.
使用四种α肾上腺素能激动剂(去氧肾上腺素、赛拉嗪、可乐定和去甲肾上腺素)和两种拮抗剂(哌唑嗪和育亨宾)来研究参与离体灌注犬心耳中间动脉收缩的节后α肾上腺素能受体的特性。所有激动剂在灌注动脉制剂中诱导血管收缩的效力几乎相等(即,所有激动剂均以剂量相关的方式引起强烈的血管收缩反应;每种激动剂的阈剂量在0.003至0.01微克的剂量范围内,每种药物0.3至1.0微克可使灌注压升高约200毫米汞柱)。哌唑嗪以竞争性方式抑制去氧肾上腺素诱导的血管收缩,但育亨宾对去氧肾上腺素诱导的反应没有显著影响。赛拉嗪诱导的反应可被哌唑嗪和育亨宾抑制,但前者在低剂量时效力低于后者,且哌唑嗪对赛拉嗪的拮抗特性不具有竞争性。哌唑嗪对去氧肾上腺素、赛拉嗪和可乐定的pA2值分别为7.10、6.82和6.99,育亨宾对赛拉嗪的pA2值为7.16。这些结果支持了这样一种理论,即不仅α-1而且α-2肾上腺素能受体都参与了离体灌注犬心耳中间动脉的收缩反应。