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介导胆囊收缩素对禽类小肠纵行平滑肌作用的机制。

Mechanisms mediating the effects of cholecystokinin on avian small intestine longitudinal smooth muscle.

作者信息

Martín M T, Fernández E, Fernández A G, Goñalons E

机构信息

Department of Physiology and Cell Biology, Universitat Autònoma de Barcelona, Bellaterra, Spain.

出版信息

Regul Pept. 1994 May 5;51(2):91-9. doi: 10.1016/0167-0115(94)90198-8.

Abstract

The aims of this study were (1) to define the effects of CCK-8s and related peptides on chicken ileum longitudinal smooth muscle and (2) to explore the mechanisms by which such effects occur. The effects of CCK-8s were assayed in vitro on chicken longitudinal ileal strips. CCK-8s produced contraction of ileal strips (EC50 8.8.10(-9) M). CCK-8ns and CCK-4 did not have remarkable contractile effects even when added at concentrations 200-times higher than the EC50 for CCK-8s. L365,260 slightly inhibited the effects of CCK-8s whereas L364,718 was ineffective. Tetrodotoxin (10(-6) M) markedly decreased the effects of CCK-8s. Atropine (10(-6) M) did not modify the neurally mediated effects of CCK-8s, whereas ketanserin (10(-5) M) decreased the response to CCK-8s. Substance P-desensitized preparations exhibited reduced responses to CCK-8s. Our results indicate that CCK receptors present in chicken ileum behave similarly but not identically to the CCK-A receptor described in mammals. Most of these CCK receptors are neurally located but a minor proportion is also present on smooth muscle. The neurally mediated response to CCK-8s does not involve cholinergic mechanisms, but serotonin and substance P releasing neurons.

摘要

本研究的目的是

(1)确定胆囊收缩素八肽(CCK-8s)及相关肽对鸡回肠纵行平滑肌的作用;(2)探究这些作用产生的机制。在体外对鸡回肠纵行肌条测定CCK-8s的作用。CCK-8s可使回肠肌条收缩(半数有效浓度[EC50]为8.8×10⁻⁹ M)。即使以高于CCK-8s的EC50 200倍的浓度添加,CCK-8去硫酸化肽(CCK-8ns)和CCK-4也没有显著的收缩作用。L365,260可轻微抑制CCK-8s的作用,而L364,718则无效。河豚毒素(10⁻⁶ M)可显著降低CCK-8s的作用。阿托品(10⁻⁶ M)不会改变CCK-8s的神经介导作用,而酮色林(10⁻⁵ M)可降低对CCK-8s的反应。P物质脱敏制剂对CCK-8s的反应降低。我们的结果表明,鸡回肠中存在的CCK受体与哺乳动物中描述的CCK-A受体表现相似但并不完全相同。这些CCK受体大多数位于神经上,但也有一小部分存在于平滑肌上。对CCK-8s的神经介导反应不涉及胆碱能机制,而是涉及5-羟色胺和P物质释放神经元。

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