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小鼠输精管中介导收缩的α2肾上腺素能受体。

Contraction-mediating alpha 2-adrenoceptors in the mouse vas deferens.

作者信息

Bültmann R, von Kügelgen I, Starke K

机构信息

Pharmakologisches Institut, Freiburg, Federal Republic of Germany.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1991 Jun;343(6):623-32. doi: 10.1007/BF00184294.

Abstract

The question of the existence of postjunctional, contraction-mediating alpha 2-adrenoceptors, in addition to the known alpha 1-adrenoceptors, was studied in the mouse isolated vas deferens. Both the alpha 1-selective agonist phenylephrine and the alpha 2-selective agonist 5-bromo-6-(2-imidazolin-2-ylamino)-quinoxaline (UK 14,304) caused contraction of the vas deferens. In the presence of the alpha 1-selective antagonist prazosin (added in order to prevent an alpha 1 component in the effect of high concentrations of UK 14,304), the alpha 2-selective antagonist yohimbine and idazoxan shifted the concentration-response curve of UK 14,304 to the right in a manner compatible with competitive antagonism and with dissociation constants KB indicating the involvement of alpha 2-adrenoceptors. The maximal contraction elicited by UK 14,304 (in the presence of prazosin) was much lower than the maximal contraction elicited by phenylephrine. The effect of UK 14,304 was not changed by the P2-purinoceptor agonist alpha,beta-methylene-ATP and was reduced by neuropeptide Y, but was markedly enhanced by relatively low concentrations of phenylephrine. When the sympathetic fibres of the vas deferens were stimulated by trains of ten widely spaced (0.5 Hz) electric pulses, the tissue responded with ten separate twitches in which purinergic and adrenergic components were isolated by prazosin and suramin, respectively. Prazosin reduced the first adrenergic twitch in these trains at concentrations close to its KB value at alpha 1-adrenoceptors, whereas yohimbine and idazoxan reduced the first adrenergic twitch at concentrations far lower than their KB values at alpha 1-adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

除了已知的α1肾上腺素能受体外,在小鼠离体输精管中研究了是否存在节后收缩介导的α2肾上腺素能受体。α1选择性激动剂去氧肾上腺素和α2选择性激动剂5-溴-6-(2-咪唑啉-2-基氨基)喹喔啉(UK 14,304)均可引起输精管收缩。在α1选择性拮抗剂哌唑嗪存在的情况下(添加哌唑嗪是为了防止高浓度UK 14,304的作用中出现α1成分),α2选择性拮抗剂育亨宾和咪唑克生使UK 14,304的浓度-反应曲线右移,其方式符合竞争性拮抗作用,解离常数KB表明α2肾上腺素能受体参与其中。UK 14,304(在哌唑嗪存在下)引起的最大收缩远低于去氧肾上腺素引起的最大收缩。UK 14,304的作用不受P2嘌呤能受体激动剂α,β-亚甲基ATP的影响,但可被神经肽Y减弱,但相对低浓度的去氧肾上腺素可使其明显增强。当以一系列间隔较宽(0.5 Hz)的10个电脉冲刺激输精管的交感神经纤维时,组织会产生10次单独的抽搐,其中嘌呤能和肾上腺素能成分分别被哌唑嗪和苏拉明分离。哌唑嗪在接近其在α1肾上腺素能受体处的KB值的浓度下可降低这些系列中的第一次肾上腺素能抽搐,而育亨宾和咪唑克生在远低于其在α1肾上腺素能受体处的KB值的浓度下可降低第一次肾上腺素能抽搐。(摘要截短至250字)

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