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氨甲酰甲胆碱和胆囊收缩素八肽对猫结肠平滑肌的作用。

Effects of bethanechol and the octapeptide of cholecystokinin on colonic smooth muscle in the cat.

作者信息

Snape W J, Tan S T, Kao H W

出版信息

Am J Physiol. 1987 May;252(5 Pt 1):G654-61. doi: 10.1152/ajpgi.1987.252.5.G654.

DOI:10.1152/ajpgi.1987.252.5.G654
PMID:2883898
Abstract

The aim of this study is to compare the action of the cholinergic agonist, bethanechol, with the action of the octapeptide of cholecystokinin (CCK-OP) on feline circular colonic smooth muscle membrane potential and isometric tension, using the double sucrose gap. Depolarization of the membrane greater than 10 mV by K+ or bethanechol increased tension and spontaneous spike activity. CCK-OP (10(-9) M) depolarized the membrane (6.1 +/- 1.3 mV) without an increase in tension or spike activity. Depolarization of the membrane by increasing [K+]o was associated with a decrease in the membrane resistance. The slow-wave duration (2.3 +/- 0.2 s) was unchanged by administration of K+ or bethanechol but was prolonged after increasing concentrations of CCK-OP. The maximum effect occurred at a 10(-10) M concentration of CCK-OP (4.5 +/- 0.4 s, P less than 0.01). At higher concentrations of CCK-OP (greater than 10(-10) M), the slow-wave pattern became disorganized. Addition of increasing concentrations of [K+]o or bethanechol, but not CCK-OP, stimulated a concentration-dependent increase in the maximum rate of rise (dV/dtmax) of an evoked spike potential. These studies suggest 1) bethanechol decreased the membrane potential without altering the slow-wave activity, whereas CCK-OP has a minimal effect on the membrane potential but distorted the slow-wave shape; 2) an increased amplitude of the spike and dV/dtmax of the spike were associated with an increase in phasic contractions after bethanechol or increased [K+]o; 3) the lack of an increase in the spike amplitude and the dV/dtmax to CCK-OP was associated with no increase in phasic contraction.

摘要

本研究的目的是使用双蔗糖间隙法,比较胆碱能激动剂氨甲酰甲胆碱与胆囊收缩素八肽(CCK-OP)对猫结肠环形平滑肌膜电位和等长张力的作用。钾离子或氨甲酰甲胆碱使膜去极化超过10 mV会增加张力和自发峰电位活动。CCK-OP(10⁻⁹ M)使膜去极化(6.1±1.3 mV),但不增加张力或峰电位活动。通过增加细胞外钾离子浓度使膜去极化与膜电阻降低有关。给予钾离子或氨甲酰甲胆碱后,慢波持续时间(2.3±0.2秒)未改变,但在增加CCK-OP浓度后延长。最大效应出现在CCK-OP浓度为10⁻¹⁰ M时(4.5±0.4秒,P<0.01)。在更高浓度的CCK-OP(大于10⁻¹⁰ M)时,慢波模式变得紊乱。增加细胞外钾离子浓度或氨甲酰甲胆碱的浓度,但不增加CCK-OP的浓度,会刺激诱发峰电位的最大上升速率(dV/dtmax)呈浓度依赖性增加。这些研究表明:1)氨甲酰甲胆碱降低膜电位而不改变慢波活动,而CCK-OP对膜电位影响最小,但会扭曲慢波形状;2)氨甲酰甲胆碱或增加细胞外钾离子浓度后,峰电位幅度增加和峰电位dV/dtmax增加与相性收缩增加有关;3)CCK-OP使峰电位幅度和dV/dtmax不增加与相性收缩不增加有关。

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