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M3 毒蕈碱受体在豚鼠胃环形肌中与三种不同的转导机制相连,且具有不同的效能。

The M3 muscarinic receptor links to three different transduction mechanisms with different efficacies in circular muscle of guinea-pig stomach.

作者信息

Parekh A B, Brading A F

机构信息

University Department of Pharmacology, Oxford.

出版信息

Br J Pharmacol. 1992 Jul;106(3):639-43. doi: 10.1111/j.1476-5381.1992.tb14388.x.

Abstract
  1. In a previous publication, we showed that 10 microM carbachol induced contraction by activating three independent transduction mechanisms in circular smooth muscle of guinea-pig gastric fundus (Parekh & Brading, 1991). These were: inositol trisphosphate-mediated intracellular Ca2+ release, Ca2+ influx through a nifedipine-sensitive route and Ca2+ influx through a receptor operated nifedipine-insensitive pathway. The former two processes contribute to the phasic contraction and the latter two to the tonic contraction. In this paper, we have studied the effects of muscarinic receptor antagonists with known selectivity for different muscarinic receptor subtypes, on the contraction evoked by 10 microM carbachol. 2. Low concentrations of pirenzepine (M1 selective) had little effect on the contraction initiated by carbachol. Higher concentrations (greater than 1 microM) reduced only the phasic component. This concentration of pirenzepine greatly reduced the contraction evoked by 10 microM carbachol in Ca(2+)-free solution, indicating inhibition of intracellular Ca2+ release. 3. In the presence of 10 microM nifedipine, the tonic contraction evoked by 10 microM carbachol (reflecting the receptor-operated nifedipine-insensitive route) was abolished by 10 microM pirenzepine. In the absence of nifedipine pretreatment, however, 10 microM pirenzepine did not abolish the contraction to 10 microM carbachol. This contraction was subsequently abolished by nifedipine. 4. Only high concentrations (greater than 10 microM) of the M2-selective antagonist, gallamine, inhibited the contraction to 10 microM carbachol. Like pirenzepine, gallamine preferentially inhibited the phasic component of the contraction, indicating an effect on intracellular Ca2+ release. 5. The non-selective muscarinic receptor antagonist, atropine, abolished all components of the contraction. At low concentrations, atropine also reduced the phasic component without affecting the tonic one, indicating preferential inhibition of intracellular Ca2+ release.6. It is concluded that (i) the different transduction mechanisms have different sensitivities to the antagonists used and (ii) an M3 receptor activates the three transduction mechanisms with different efficacies.
摘要
  1. 在之前的一篇论文中,我们发现10微摩尔的卡巴胆碱通过激活豚鼠胃底环行平滑肌中的三种独立转导机制来诱发收缩(帕雷克和布雷丁,1991年)。这三种机制分别是:肌醇三磷酸介导的细胞内钙离子释放、通过硝苯地平敏感途径的钙离子内流以及通过受体操纵的硝苯地平不敏感途径的钙离子内流。前两种过程导致相性收缩,后两种导致紧张性收缩。在本文中,我们研究了对不同毒蕈碱受体亚型具有已知选择性的毒蕈碱受体拮抗剂对10微摩尔卡巴胆碱诱发的收缩的影响。2. 低浓度的哌仑西平(M1选择性)对卡巴胆碱引发的收缩影响很小。较高浓度(大于1微摩尔)仅降低相性成分。该浓度的哌仑西平在无钙溶液中极大地降低了10微摩尔卡巴胆碱诱发的收缩,表明抑制了细胞内钙离子释放。3. 在存在10微摩尔硝苯地平的情况下,10微摩尔哌仑西平消除了10微摩尔卡巴胆碱诱发的紧张性收缩(反映受体操纵的硝苯地平不敏感途径)。然而,在没有硝苯地平预处理的情况下,10微摩尔哌仑西平并未消除对10微摩尔卡巴胆碱的收缩。随后硝苯地平消除了这种收缩。4. 只有高浓度(大于10微摩尔)的M2选择性拮抗剂加拉明抑制对10微摩尔卡巴胆碱的收缩。与哌仑西平一样,加拉明优先抑制收缩的相性成分,表明对细胞内钙离子释放有影响。5. 非选择性毒蕈碱受体拮抗剂阿托品消除了收缩的所有成分。在低浓度时,阿托品也降低了相性成分而不影响紧张性成分,表明优先抑制细胞内钙离子释放。6. 得出的结论是:(i)不同的转导机制对所用拮抗剂具有不同的敏感性;(ii)M3受体以不同的效力激活这三种转导机制。

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