A muscarinic receptor subtype modulates vagally stimulated bronchial contraction.
A muscarinic receptor subtype modulates vagally stimulated bronchial contraction.
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毒蕈碱受体亚型调节迷走神经刺激的支气管收缩。
DOI：
10.1152/jappl.1988.65.5.2144
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Halonen,M
中科院分区：
文献类型：
--
作者：
Bloom,JW;Baumgartener-Folkerts,C;Palmer,JD;Yamamura,HI;Halonen,M
开发了一种体外制剂来研究迷走神经刺激（节前）和场刺激（节后）兔主干支气管的收缩，并比较毒蕈碱拮抗剂对该收缩的抑制作用。阿托品 (60 nM) 完全消除了场刺激或迷走神经刺激的最大收缩反应（20 V、0.5 ms、64 Hz）。六甲铵 (0.1 mM) 消除了对迷走神经刺激的反应，但不影响场刺激反应。为了比较阿托品和哌仑西平作为神经平滑肌连接处拮抗剂的有效性，进行了场刺激收缩的抑制研究。与产生 25%、50% 和 75% 抑制（分别为 IC25、IC50 和 IC75）的拮抗剂的抑制浓度相比，哌仑西平的效力比阿托品低 102 至 178 倍，表明神经-平滑肌连接处的毒蕈碱受体是对哌仑西平（M2 亚型）亲和力低的毒蕈碱受体。阿托品对迷走神经和场刺激的收缩具有类似的抑制作用。相反，哌仑西平在抑制迷走神经刺激收缩方面比场刺激收缩更有效，尤其是在IC25时，哌仑西平在抑制迷走神经刺激收缩方面的效力仅比阿托品低8至22倍。这些数据表明毒蕈碱受体的 M1 亚型通过支气管副交感神经节调节兴奋性神经传递。
An in vitro preparation was developed to study vagus nerve-stimulated (preganglionic) and field-stimulated (post-ganglionic) contraction of the rabbit main stem bronchus and to compare the inhibitory effects of muscarinic antagonists on that contraction. The maximal contractile responses (20 V, 0.5 ms, 64 Hz) for either field or vagal stimulation were completely abolished by atropine (60 nM). Hexamethonium (0.1 mM) abolished the response to vagal stimulation but did not affect the field-stimulated response. To compare the effectiveness of atropine and pirenzepine as antagonists at the nerve-smooth muscle junction, inhibition studies of field-stimulated contractions were performed. Pirenzepine was 102- to 178-fold less potent than atropine when compared at the inhibitory concentration of antagonist that produced 25, 50, and 75% inhibition (IC25, IC50, and IC75, respectively), indicating that the muscarinic receptor at the nerve-smooth muscle junction is a muscarinic receptor with low affinity for pirenzepine (M2 subtype). Atropine had similar inhibitory effects on vagal- and field-stimulated contractions. In contrast, pirenzepine was more potent in inhibiting vagally stimulated contraction than field-stimulated contraction, especially at the IC25 where pirenzepine was only 8- to 22-fold less potent than atropine in inhibiting vagally stimulated contraction. These data suggest that an M1 subtype of muscarinic receptor modulates excitatory neurotransmission through bronchial parasympathetic ganglia.
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