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机构地区:[1]第四军医大学药理教研室
出 处:《中国药理学报》1994年第1期60-64,共5页Acta Pharmacologica Sinica
摘 要:(R)-α-甲基组胺(α-MeHA)低浓度抑制,高浓度增强电场刺激诱发的离体输精管收缩。上述效应可分别被thioperamide和氯苯那敏拮抗,Pyridelethyl-amine(Pyr)能增强电场刺激诱发的输精管收缩,α-MeHA和Pyr对于直接电刺激或去甲肾上腺素(NE)诱发的输精管收缩均无影响,以上表明,豚鼠输精管交感神经末稍分布有组胺H_3和H_1两种受体,它们分别介导抑制和促进NE的释放。The action of (R)-a-methylhistamine (a-MeHA), a selective H3-receptor agonist, on field stimulation induced contraction of guinea pig vas deferens was composed of 2 components: the 'inhibition' (0. 1 -100 nmon·L-1) and the 'enhancement' (1 - 10 μmol·L-1). In the presence of histamine H1 antagonist, chlorpheniramine (1 μmol·L-1), a-MeHA (0.1 nmol·L-1 - 10 μmol·L-1) showed only a concentration-dependent inhibition. Selective histamine H3-receptor antagonist, thioperamide (1 nmol·L-1- 10 μmol · L-1 ) antagonized the inhibitory effect of a-MeHA and increased the contractile amplitude of vas deferens elicited by field pulses when thioperamide was used alone. a-MeHA 10 μmol·L-1 enhanced the contractile amplitude, which was reversed by chlorpheniramine 1 μmol·L-1, but not by ranitidine (1 μmol · L-1 ). Pyridelethylamine, an H1-receptor agonist, facilitated concentration-dependently the contractile response of vas deferens. The effect was antagonized by chlorpheniramine, but not by ranitidine. Dimaprit, an H2-receptor agonist had no effect on the field stimulation induced sympathetic response. Both a-MeHA and pyridelethylamine failed to influence the contraction of 'MS deferens elicited by direct field stimulation in smooth muscle or by exogenously applied nore-pinephrine. It was concluded that histamine H1- and H3-receptors existed in sympathetic terminals of guinea pig vas deferens and facilitated or inhibited the sympathetic neurotransmission.
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