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毒蕈碱型乙酰胆碱受体在猫十二指肠一氧化氮途径中的作用。

Participation of muscarinic acetylcholine receptors in nitric oxide pathway in cat duodenum.

作者信息

Shikova L I, Kortezova N I

机构信息

Institute of Physiology, Bulgarian Academy of Sciences, Sofia, Bulgaria.

出版信息

Acta Physiol Pharmacol Bulg. 2000;25(2):57-61.

Abstract

The effect of activation of muscarinic acetylcholine subtype M1 receptors on the electrical field stimulation (EFS)-induced contractions in cat duodenal muscle strips was investigated. EFS elicited two types of responses: a) on-contraction; and b) off-contraction. The EFS-evoked responses were tetrodotoxin- and atropine-sensitive. In all strips the muscarinic acetylcholine subtype M1 agonist (4-Hydroxy-2-butynyl)-1-trimethylammonium-m-chlorocarbanilate chloride (McN-A-343) increased the tone and the amplitude of the spontaneous contractions. On this background EFS produced an inhibition of the phasic contractions at switching on the stimulation, followed by off-contractions. The EFS-induced inhibition was removed by N omega-nitro-L-arginine and was partly overcome by L-arginine. The results suggest the participation of muscarinic acetylcholine subtipe M1 receptors in the mediation of nitrergic inhibitory responses in cat duodenum.

摘要

研究了毒蕈碱型乙酰胆碱M1受体激活对猫十二指肠肌条电场刺激(EFS)诱导收缩的影响。EFS引发两种反应:a)刺激时收缩;b)刺激停止时收缩。EFS诱发的反应对河豚毒素和阿托品敏感。在所有肌条中,毒蕈碱型乙酰胆碱M1激动剂(4-羟基-2-丁炔基)-1-三甲基氯化铵间氯卡巴腙(McN-A-343)增加了自发收缩的张力和幅度。在此基础上,EFS在刺激开始时抑制了相性收缩,随后出现刺激停止时收缩。EFS诱导的抑制作用被Nω-硝基-L-精氨酸消除,部分被L-精氨酸克服。结果表明毒蕈碱型乙酰胆碱M1受体参与了猫十二指肠中一氧化氮能抑制反应的介导。

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