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St-587对大鼠离体输精管α-肾上腺素能受体的影响。

Effects of St-587 on the alpha-adrenoceptors in the bisected rat vas deferens.

作者信息

Badia A, Sallés J

机构信息

Departament de Farmacologia i Psiquiatria, Universitat Autònoma de Barcelona, Spain.

出版信息

J Pharm Pharmacol. 1989 Sep;41(9):612-6. doi: 10.1111/j.2042-7158.1989.tb06541.x.

Abstract

The effects of the alpha-adrenoceptor agonist St-587 have been studied on the twitch responses induced by field stimulation in the prostatic portion of rat vas deferens. Moreover the drug's influence on the unstimulated prostatic and epididymal halves of rat vas deferens has also been determined. Alone and after addition of yohimbine (0.3 microM) it enhanced in a concentration-dependent manner the twitch responses in the prostatic half. Prazosin competitively antagonized (pA2 = 8.41 +/- 0.03) this effect. The enhancing effect of St-587 was not reduced in reserpinized animals. These results suggest that post-synaptic alpha 1-adrenoceptors are involved in the potentiation of twitch responses induced by St-587. When alpha 1-adrenoceptors were blocked by prazosin (0.1 microM), St-587 partially inhibited the twitch responses of the prostatic portion of rat vas deferens (Emax = 49.5 +/- 3.5%). Yohimbine completely reversed the inhibitory effects of both St-587 and clonidine. Furthermore St-587 antagonized the inhibitory effects of clonidine on twitch responses. Thus it appears that St-587 also behaves as a partial agonist of presynaptic alpha 2-adrenoceptors in this portion of rat vas deferens, but it did not induce contractions in the unstimulated prostatic half of the vas deferens. However, it competitively antagonized the alpha 1-adrenoceptor agonist phenylephrine by acting as an antagonist of prostatic postsynaptic alpha 1 adrenoceptors. These alpha 1-adrenoceptors are probably different from those that mediate the twitch enhancing response to St-587 in that portion. On the other hand, St-587 was a partial agonist of alpha 1-adrenoceptors in the epididymal half.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

已研究了α-肾上腺素能受体激动剂St-587对大鼠输精管前列腺部电场刺激诱发的抽搐反应的影响。此外,还确定了该药物对大鼠输精管未受刺激的前列腺段和附睾段的影响。单独使用及添加育亨宾(0.3微摩尔)后,它以浓度依赖性方式增强了前列腺段的抽搐反应。哌唑嗪竞争性拮抗(pA2 = 8.41±0.03)此效应。在利血平化的动物中,St-587的增强作用未降低。这些结果表明,突触后α1-肾上腺素能受体参与了St-587诱发的抽搐反应的增强。当α1-肾上腺素能受体被哌唑嗪(0.1微摩尔)阻断时,St-587部分抑制大鼠输精管前列腺部的抽搐反应(最大效应=49.5±3.5%)。育亨宾完全逆转了St-587和可乐定的抑制作用。此外,St-587拮抗可乐定对抽搐反应的抑制作用。因此,在大鼠输精管的这一部分,St-587似乎也表现为突触前α2-肾上腺素能受体的部分激动剂,但它并未在输精管未受刺激的前列腺段诱发收缩。然而,它通过作为前列腺突触后α1肾上腺素能受体的拮抗剂,竞争性拮抗α1-肾上腺素能受体激动剂去氧肾上腺素。这些α1-肾上腺素能受体可能与介导该部分对St-587抽搐增强反应的受体不同。另一方面,St-587是附睾段α1-肾上腺素能受体的部分激动剂。(摘要截短于250字)

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