Hashitani H, Suzuki H
Department of Physiology, Nagoya City University Medical School, Japan.
Eur J Pharmacol. 1995 Sep 15;284(1-2):177-83. doi: 10.1016/0014-2999(95)00386-y.
In smooth muscles of the guinea-pig bladder, intramural nerve stimulation generated an excitatory junctional potential (e.j.p.), action potential and twitch contraction. Nicardipine inhibited the action potential but not the e.j.p. The e.j.p. amplitude was reduced by suramin, or desensitization of the ATP receptor with receptor agonists. The amplitude of the twitch contraction was reduced by atropine, and the remainder was blocked by nicardipine. In the presence of maximally effective concentrations of atropine, the threshold concentration of acetylcholine required to produce contraction was about 10(-7) M, whereas acetylcholine concentrations greater than 10(-6) M were required to cause depolarization. It is concluded that nerve stimulation releases acetylcholine and ATP, and the former produces contraction without change in the membrane potential, while the latter generates the e.j.p. which triggers an action potential and thus elicits contractions.
在豚鼠膀胱的平滑肌中，壁内神经刺激可产生兴奋性接头电位（e.j.p.）、动作电位和抽搐收缩。尼卡地平抑制动作电位，但不抑制e.j.p.。苏拉明或用受体激动剂使ATP受体脱敏可降低e.j.p.的幅度。阿托品可降低抽搐收缩的幅度，其余部分则被尼卡地平阻断。在存在最大有效浓度阿托品的情况下，产生收缩所需的乙酰胆碱阈值浓度约为10^(-7) M，而引起去极化则需要大于10^(-6) M的乙酰胆碱浓度。结论是神经刺激释放乙酰胆碱和ATP，前者在膜电位不变的情况下产生收缩，而后者产生e.j.p.，触发动作电位，从而引发收缩。
