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参与兔小肠收缩性的钾离子通道。

K+ channels involved in contractility of rabbit small intestine.

作者信息

Lamarca V, Grasa L, Fagundes D S, Arruebo M P, Plaza M A, Murillo M D

机构信息

Departamento de Farmacología y Fisiologia (Fisiologia), Facultad de Veterinaria, Universidad de Zaragoza, Miguel Servet 177, 50013 Zaragoza, Spain.

出版信息

J Physiol Biochem. 2006 Dec;62(4):227-36. doi: 10.1007/BF03165751.

Abstract

Most excitable cells, including gastrointestinal smooth muscle cells, express several types of K+ channels. The aim of this study was to examine the types of K' channels involved in the contractility of longitudinal smooth muscle of rabbit small intestine in vitro. Spontaneous contractions and KCl-stimulated contractions were reduced by atropine, phentolamine, propranolol, suramin, tetrodotoxin and indomethacin. The amplitude and tone of spontaneous contractions were increased by apamin, charybdotoxin, iberiotoxin, E4031, tetraetylammonium (TEA) and BaCl2. The frequency of contractions was reduced in the presence of apamin and TEA and increased by charybdotoxin. It was found that 4-aminopyridine increased the tone of spontaneous contractions and reduced the amplitude and frequency of contractions. Glibenclamide did not modify the amplitude, frequency or tone of contractions. KCl-stimulated contractions were increased by E4031, were not modified by apamin, glibenclamide, NS1619 or diazoxide, and were reduced by charybdotoxin, TEA, 4-aminopyridine or BaCl2. These results suggest that both Ca2+-activated K+ channels of small and high conductance, and HERG K+ channels and inward rectifier K+ channels participate in spontaneous contractions of small intestine. On the other hand, voltage-dependent K+ channels, HERG K+ channels, inward rectifier K+ channels and high conductance Ca2+-activated K+ channels are involved in KCl-stimulated contractions.

摘要

大多数可兴奋细胞,包括胃肠道平滑肌细胞,都表达几种类型的钾离子通道。本研究的目的是检测体外培养的兔小肠纵行平滑肌收缩性所涉及的钾离子通道类型。阿托品、酚妥拉明、普萘洛尔、苏拉明、河豚毒素和吲哚美辛可降低自发收缩和氯化钾刺激的收缩。蜂毒明肽、蝎毒素、iberiotoxin、E4031、四乙铵(TEA)和氯化钡可增加自发收缩的幅度和张力。在蜂毒明肽和TEA存在的情况下,收缩频率降低,而蝎毒素可使其增加。发现4-氨基吡啶可增加自发收缩的张力,并降低收缩的幅度和频率。格列本脲不改变收缩的幅度、频率或张力。E4031可增加氯化钾刺激的收缩,蜂毒明肽、格列本脲、NS1619或二氮嗪对其无影响,而蝎毒素、TEA、4-氨基吡啶或氯化钡可降低该收缩。这些结果表明,小电导和大电导的钙激活钾通道、HERG钾通道和内向整流钾通道均参与小肠的自发收缩。另一方面,电压依赖性钾通道、HERG钾通道、内向整流钾通道和大电导钙激活钾通道参与氯化钾刺激的收缩。

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