Trendelenburg Anne-Ulrike, Gomeza Jesus, Klebroff Werner, Zhou Hongxia, Wess Jürgen
Institut für Experimentelle und Klinische Pharmakologie und Toxikologie, Albertstrasse 25, D-79104 Freiburg, Germany.
Br J Pharmacol. 2003 Feb;138(3):469-80. doi: 10.1038/sj.bjp.0705053.
1 Presynaptic muscarinic receptors modulate sympathetic transmitter release. The goal of the present study was to identify the muscarinic receptor subtype(s) mediating inhibition of sympathetic transmitter release in mouse atria, urinary bladder and vas deferens. To address this question, electrically evoked noradrenaline release was assessed using tissue preparations from NMRI, M(2)- and M(4)-knockout, and the corresponding M(2)- and M(4)-wildtype mice, after preincubation with (3)H-noradrenaline. 2 The muscarinic agonist carbachol decreased evoked tritium overflow (20 pulses/50 Hz) in each tissue and strain investigated. After deletion of the M(2)-receptor the maximal inhibition by carbachol was significantly reduced (by 41-72%), but not abolished, in all tissues. After deletion of the M(4)-receptor a moderate and significant reduction of the maximal inhibition by carbachol (by 28%) was observed only in the vas deferens. 3 Experiments with the muscarinic antagonists methoctramine and pirenzepine confirmed that the presynaptic muscarinic receptors were predominantly M(2) in atria and bladder and probably a mixture of M(2) and M(4) in the vas deferens. 4 Experiments in the urinary bladder with the cholinesterase inhibitor physostigmine and the muscarinic antagonist ipratropium demonstrated that endogenously released acetylcholine predominantly acted through M(2)-receptors to inhibit noradrenaline release. However, the results do not exclude a minor contribution of M(4)-receptors to this endogenous inhibition. 5 In conclusion, our results clearly indicate that the release-inhibiting muscarinic receptors on postganglionic sympathetic axons in mouse atria, bladder and vas deferens represent mixtures of M(2)- and non-M(2)-receptors. The non-M(2)-receptors remain unknown in atria and the bladder, and may represent primarily M(4)-receptors in the vas deferens. These results reveal an unexpected heterogeneity among the muscarinic receptors mediating inhibition of noradrenaline release.
1 突触前毒蕈碱受体调节交感神经递质释放。本研究的目的是确定介导小鼠心房、膀胱和输精管中交感神经递质释放抑制作用的毒蕈碱受体亚型。为解决这个问题,在与(3)H-去甲肾上腺素预孵育后,使用来自NMRI、M(2)-和M(4)-基因敲除小鼠以及相应的M(2)-和M(4)-野生型小鼠的组织标本,评估电诱发的去甲肾上腺素释放。
2 毒蕈碱激动剂卡巴胆碱降低了所研究的每个组织和品系中诱发的氚溢出(20次脉冲/50Hz)。在缺失M(2)-受体后,卡巴胆碱的最大抑制作用在所有组织中均显著降低(降低41%-72%),但并未消除。在缺失M(4)-受体后,仅在输精管中观察到卡巴胆碱最大抑制作用的中度且显著降低(降低28%)。
3 使用毒蕈碱拮抗剂甲硫卡巴胆碱和哌仑西平的实验证实,突触前毒蕈碱受体在心房和膀胱中主要是M(2)型,在输精管中可能是M(2)和M(4)的混合物。
4 在膀胱中使用胆碱酯酶抑制剂毒扁豆碱和毒蕈碱拮抗剂异丙托溴铵的实验表明,内源性释放的乙酰胆碱主要通过M(2)-受体起作用以抑制去甲肾上腺素释放。然而,结果并不排除M(4)-受体对这种内源性抑制作用有较小贡献。
5 总之,我们的结果清楚地表明,小鼠心房、膀胱和输精管中节后交感神经轴突上抑制释放的毒蕈碱受体是M(2)-受体和非M(2)-受体的混合物。心房和膀胱中的非M(2)-受体尚不清楚,在输精管中可能主要是M(4)-受体。这些结果揭示了介导去甲肾上腺素释放抑制作用的毒蕈碱受体之间出人意料的异质性。