ELECTRICAL AND MECHANICAL-ACTIVITY RECORDED FROM RABBIT URINARY-BLADDER IN RESPONSE TO NERVE-STIMULATION
ELECTRICAL AND MECHANICAL-ACTIVITY RECORDED FROM RABBIT URINARY-BLADDER IN RESPONSE TO NERVE-STIMULATION
复制标题
DOI：
10.1113/jphysiol.1983.sp014666
复制
发表时间：
1983-01-01
影响因子：
5.5
通讯作者：
ITO, Y
中科院分区：
文献类型：
--
作者：
CREED, KE;ISHIKAWA, S;ITO, Y
用微电极法和双蔗糖间隙法研究了家兔膀胱平滑肌膜对肌内神经刺激的反应。细胞产生有规律的自发动作电位。乙酰胆碱产生的维持增加的频率，和ATP的短暂增加。去甲肾上腺素（norepinephrine）仅在非常高的浓度下增加频率。施加短电流脉冲（50 μ s）产生具有叠加尖峰的初始兴奋性结电位（ejp），随后是晚期去极化。在某些情况下，膜的超极化出现在初始ejp和晚期去极化之间。所有这些反应都被河豚毒素所消除。用新斯的明预处理可使晚期去极化增强，而阿托品可使其消失。这意味着延迟的去极化是由于毒蕈碱受体的激活。当晚期去极化消失时，超极化幅度增加。乙啶、酚妥拉明、甲基麦角新碱、美托咪胺、奎尼丁和茶碱均不影响ejp和收缩。这意味着ejp不是由肾上腺素能、色胺能、组胺能或嘌呤能受体的激活介导的。ATP由于膜去极化和膜电阻降低而降低了ejp的振幅。重复刺激（0.5- 2.0Hz）可使Ejp的幅度逐渐降低。然而，在ATP的存在下，抑郁症的发生率没有变化。双嘧达莫没有改变电场刺激的电和机械反应。这些结果不支持ATP是非胆碱能兴奋性递质的提议。阿帕明和四乙铵（TEA）抑制场刺激产生的超极化，但乙啶不抑制超极化。超极化是由于膜的K电导增加，但它是不可能得出结论，是否该组件是由于神经递质的抑制作用或仅后超极化的尖峰。显然，兔膀胱接受胆碱能和非胆碱能兴奋性神经元。
Responses of the smooth muscle membrane of the rabbit bladder to intramuscular nerve stimulation were investigated by the microelectrode and double sucrose-gap methods. The cell generated regular spontaneous action potentials. Acetylcholine produced a maintained increase in the frequency, and ATP a transient increase. Noradrenaline [norepinephrine] only increased the frequency at very high concentrations. Application of short current pulses (50 .mu.s) produced an initial excitatory junction potential (ejp) with a superimposed spike, followed by a late depolarization. On some occasions, hyperpolarization of the membrane appeared between initial ejp and the late depolarization. All these responses were abolished by tetrodotoxin. The late depolarization was enhanced by pretreatment with neostigmine and abolished by atropine. This means that the delayed depolarization is due to activation of the muscarinic receptor. When the late depolarization was abolished, the amplitude of hyperpolarization was enhanced. The ejp and contraction were unaffected by guanethidine, phentolamine, methylsergide, mepyramine, quinidine or theophylline. This means that the ejp is not mediated by activation of adrenergic, tryptaminergic, histaminergic or purinergic receptors. ATP reduced the amplitude of the ejp due to depolarization of the membrane and reduction in the membrane resistance. The amplitude of the ejp was gradually reduced by repetitive stimulation (0.5-2.0 Hz). However, the rate of depression was unchanged in the presence of ATP. Dipyridamole did not change the electrical and mechanical responses to field stimulation. These results do not support the proposal that ATP is the non-cholinergic excitatory transmitter. Apamine and tetraethylammonium (TEA) suppressed the hyperpolarization produced by field stimulation but guanethidine did not inhibit the hyperpolarization. The hyperpolarization is due to increased K conductance of the membrane, but it is not possible to conclude whether this component is due to the inhibitory action of a neurotransmitter or solely to after hyperpolarization of the spike. Apparently the rabbit bladder receives both cholinergic and noncholinergic excitatory neurons.