Ionic basis for the regulation of spontaneous excitation in detrusor smooth muscle cells of the guinea-pig urinary bladder
Ionic basis for the regulation of spontaneous excitation in detrusor smooth muscle cells of the guinea-pig urinary bladder
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DOI：
10.1038/sj.bjp.0705320
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发表时间：
2003-09-01
影响因子：
7.3
通讯作者：
Brading, AF
中科院分区：
文献类型：
--
作者：
Hashitani, H;Brading, AF
采用细胞内微电极和肌张力记录技术研究了豚鼠膀胱逼尿肌平滑肌自发兴奋的调控机制逼尿肌平滑肌细胞表现出硝苯地平敏感的自发动作电位。它们的频率对膜极化高度敏感，温度降低后频率降低。降低温度也降低了自发收缩的频率并增加了其幅度Charybdotoxin （50 nm）和iberiotoxin （0.1 nm）使动作电位的振幅和持续时间增加。并在超极化（AHPs）后被废除。这两种药物也增加了自发收缩的幅度和持续时间，并减少了它们的频率。Apamin （0.1 muM）不改变动作电位的形状，但经常将单个动作电位转化为脉冲。它还增加了自发性收缩的幅度和持续时间，并降低了它们的频率。4-氨基吡啶（4-AP, 1 mM）在不影响动作电位形状的情况下增加动作电位的频率，增加自发收缩的幅度和频率环吡唑酸（CPA, 10 muM）和瑞诺定（50 muM）增加了动作电位振幅，抑制了ahp。这两种药物也增加了自发收缩的幅度和持续时间，并减少了它们的频率。1,2-(双（2-氨基苯氧基）乙烷-N，N，N‘， N’-四乙酸四基（乙酰氧基甲酯）（50 muM）显著增加动作电位的振幅和持续时间，并消除ahps逼尿肌平滑肌细胞的自发动作电位是由l型Ca2+通道打开引起的，其频率受电压依赖机制和一些代谢过程的调节。大电导Ca2+激活的K+ (BK)通道的激活和Ca2+介导的Ca2+通道的失活都参与了动作电位的复极化阶段。Ca2+通过l型Ca2+通道内流触发钙诱导的钙通过ryanodine受体释放，并激活BK通道产生ahp。小电导Ca2+激活的K+通道和电压敏感的K+通道都可能参与静息膜电位并调节动作电位的频率。动作电位的调节机制与自发性收缩的调节密切相关。
1 The regulatory mechanisms of spontaneous excitation in detrusor smooth muscles of the guinea-pig urinary bladder were investigated using intracellular microelectrode and muscle tension recording techniques.2 Detrusor smooth muscle cells exhibited nifedipine-sensitive spontaneous action potentials. Their frequency was highly sensitive to membrane polarization and was reduced by lowering the temperature. Lowering the temperature also reduced the frequency of spontaneous contractions and increased their amplitude.3 Charybdotoxin (50 nm) and iberiotoxin (0.1 muM) increased the amplitude and duration of action potentials. and abolished after hyperpolarizations (AHPs). Both agents also increased the amplitude and duration of spontaneous contractions, and reduced their frequency. Apamin (0.1 muM) did not change the shape of action potentials but often converted individual action potentials into bursts. It also increased the amplitude and duration of spontaneous contractions, and reduced their frequency. 4-aminopyrideine (4-AP, 1 mM) increased the frequency of action potentials without affecting their shape, and increased the amplitude and frequency of spontaneous contractions.4 Cyclopiazonic acid (CPA, 10 muM) and ryanodine (50 muM) increased the amplitude of action potentials, and suppressed AHPs. Both agents also increased the amplitude and duration of spontaneous contractions, and reduced their frequency. 1,2-(Bis (2-aminophenoxy) ethane-N,N,N', N'-tetraacetic acid tetrakis (acetoxymethyl ester) (50 muM) dramatically increased the amplitude and duration of the action potential, and abolished AHPs.5 Spontaneous action potentials in detrusor smooth muscles cells result from the opening of L-type Ca2+ channels, and their frequency is regulated by voltage-dependent mechanisms and by some metabolic process. Both the activation of large conductance Ca2+-activated K+ (BK) channels and Ca2+-mediated inactivation of the Ca2+ channels are involved in the repolarizing phase of action potentials. The Ca2+ influx through L-type Ca2+ channels triggers calcium-induced calcium release via ryanodine receptors and activates BK channels to generate AHPs. Both small conductance Ca2+- activated K+ channels and voltage-sensitive K+ channels may contribute to the resting membrane potential and regulate the frequency of action potentials. The regulatory mechanisms of action potentials are closely related to the regulation of spontaneous contractions.