Mechanisms underlying the electrical and mechanical responses of the guinea‐pig internal anal sphincter to field stimulation and to drugs
Mechanisms underlying the electrical and mechanical responses of the guinea‐pig internal anal sphincter to field stimulation and to drugs
复制标题
豚鼠肛门内括约肌对场刺激和药物的电和机械反应的机制
DOI：
--
复制
发表时间：
1985
影响因子：
7.3
通讯作者：
Thomas C. Muir
中科院分区：
文献类型：
--
作者：
Siew Peng Lim;Thomas C. Muir
1豚鼠肛门内括约肌的电膜特性和环行肌的反应。采用细胞内微电极和常规机械记录技术进行体外研究。2IA.A。在最初的伸展(1g)后，产生了自己的音调(3-4g)，并有明显的自发峰电位。在没有峰电位的情况下，音调下降并消失。酚妥拉明(1×10−6M)不能显著降低音调。静息膜电位为−45±3.0 mV(n=2 2 4)，空间常数(Λ)为1.13±0.1 mm(n=13)。尖峰通常超过大约15 mV。3峰电位放电频率(1~3 Hz)随膜去极化程度的不同而不同，在富K+时增加，在K+缺乏或Mn2+存在时降低。氯−-戒断对此无明显影响，但在含或不含河豚毒素(TTX；1×10−6M)的Na+缺乏溶液中，其活性明显升高。4场刺激(1~20 Hz，0.5ms，最大电压以上)产生抑制性连接电位(i.j.ps)和舒张音，高频(50 Hz或更高)时可观察到收缩，而兴奋性连接电位(e.j.ps)无收缩。阿托品(1×10−6M)、酚妥拉明(1×10−6M)或六甲基托品(1×10−6M)不能抑制肌注APP和肌松。5个I.j.ps被超极化降低，而被电流脉冲去极化增强(15 S)。Ij.p的平均平衡势。−为94 mV(相关系数γ=0.71，n=5，p<；0.001)。在K+缺乏的溶液中，I.J.P.增强，而在富K+的溶液中，I.J.P.降低。总而言之，这些结果表明，印度人民党。是由增加的GK调节的。无[Ca~(2+)]o或有Mn~(2+)(2 MM)可使ij.p消失；相反，缺乏Na~+或无Cl-−的溶液在这方面无效。6四乙基铵(5-50 mM)消除了ij.p；伴随的松弛减少了约80%。对神经刺激松弛的主要方面是由膜超极化介导的。
1 The electrical membrane characteristics and the response of the circular muscle of the guinea‐pig internal anal sphincter (i.a.s.) to field stimulation were studied in vitro using intracellular microelectrodes and conventional mechanical recording techniques. 2 The i.a.s. developed its own tone (3–4 g), following initial stretch (1 g) and spontaneous spike potentials were evident. In the absence of spike potentials, tone declined and disappeared. Tone was not significantly reduced by phentolamine (1 × 10−6 M). The resting membrane potential, measured between spontaneous spike potentials, was − 45 ± 3.0 mV (n = 224); the space constant (Λ) was 1.13 ± 0.1 mm (n = 13). Spikes usually overshot by approximately 15 mV. 3 The frequency of spike potential discharge (1–3 Hz) varied with the degree of membrane depolarization, being increased in K+‐rich and decreased in K+‐deficient solutions or by the presence of Mn2+. It was not significantly affected by Cl−‐withdrawal but was increased in Na+‐deficient solutions with or without tetrodotoxin (TTX; 1 × 10−6 M). 4 Field stimulation (1–20 Hz, 0.5 ms, supramaximal voltage) produced inhibitory junction potentials (i.j.ps) and relaxed tone; at high frequencies (50 Hz or greater), contractions were observed but excitatory junction potentials (e.j.ps) were not. I.j.ps and relaxations were inhibited by apamin (1 × 10−6M), TTX (1 × 10−6M) but not by atropine (1 × 10−6M), phentolamine (1 × 10−6M) or hexamethonium (1 × 10−6M). 5 I.j.ps were reduced by hyperpolarization and enhanced by depolarization of the membrane by current pulses (15 s). The mean equilibrium potential for the i.j.p. was − 94 mV (correlation coefficient, γ = 0.71, n = 5, p < 0.001). I.j.ps were enhanced in K+‐deficient solutions and reduced in K+‐rich solutions. Together these results suggest that the i.j.p. is mediated by an increased GK. The absence of [Ca2+]o or the presence of Mn2+ (2 mM) abolished the i.j.p.; in contrast Na+‐deficient or Cl−‐free solutions were ineffective in this respect. 6 Tetraethylammonium (5–50 mM) abolished the i.j.p.; the accompanying relaxation was reduced by about 80%. The major aspect of the relaxation to nerve stimulation is mediated by membrane hyperpolarization.