Suzuki H
J Physiol. 1985 Feb;359:401-15. doi: 10.1113/jphysiol.1985.sp015592.
Ionophoretic application of ATP to smooth muscle cells of the rabbit ear artery produced rapid depolarization of the membrane and, in the case of large doses of ATP, spike potentials or slow oscillatory potentials. The ATP response desensitized rapidly, and required over 70 s for recovery. When the intervals between repetitive application of ATP were shorter than 70 s, the amplitudes of the ATP responses successively decreased. Ejection of ATP with increasing intensities of current (10-15% of the first) was required to produce successively increasing amplitudes of ATP responses. Repetitive stimulation of perivascular nerves (at intervals of less than 10 s) evoked increasing amplitude of excitatory junction potentials (e.j.p.s). Quinidine (over 5 X 10(-5) M) inhibited and theophylline (over 5 X 10(-4) M) enhanced the ATP response, with associated depolarization or hyperpolarization of the membrane, respectively. Cocaine (over 10(-6) M) depolarized the membrane and enhanced the ATP response. Phentolamine reduced the amplitude of the ATP response with no change in the membrane potential, only when the concentration was extremely high (over 10(-4) M). These all therefore appear to represent non-specific interactions with the effects of ATP. Bath application of ATP depolarized the membrane dose dependently and, at concentrations over 5 X 10(-7) M, produced spike potentials. The amplitude of electrotonic potentials decreased during the ATP-induced depolarization, thereby suggesting an increase in ionic conductance of the membrane. ADP depolarized the membrane, the effect being weaker than that of ATP. Both AMP and adenosine hyperpolarized the membrane. The results provide evidence that in the rabbit ear artery, the e.j.p. could be mimicked by ATP. ATP can however only account for the fast e.j.p. if it is released in increasing amounts with successive nerve discharges. Reported blocking agents for ATP receptors did not block the response to ATP in this tissue.
将ATP离子电渗施加于兔耳动脉平滑肌细胞，可使细胞膜迅速去极化，大剂量ATP时可产生锋电位或缓慢振荡电位。ATP反应迅速脱敏，恢复需要70多秒。当重复施加ATP的间隔短于70秒时，ATP反应的幅度会相继降低。需要随着电流强度增加（为第一次的10 - 15%）喷射ATP，才能使ATP反应幅度相继增加。重复刺激血管周围神经（间隔小于10秒）可使兴奋性接头电位（e.j.p.s）幅度增加。奎尼丁（超过5×10⁻⁵ M）抑制，茶碱（超过5×10⁻⁴ M）增强ATP反应，分别伴有细胞膜的去极化或超极化。可卡因（超过10⁻⁶ M）使细胞膜去极化并增强ATP反应。酚妥拉明仅在浓度极高（超过10⁻⁴ M）时，才会降低ATP反应幅度而不改变膜电位。因此，这些似乎都代表了与ATP作用的非特异性相互作用。浴用ATP可使细胞膜剂量依赖性地去极化，浓度超过5×10⁻⁷ M时可产生锋电位。在ATP诱导的去极化过程中，电紧张电位的幅度降低，从而表明细胞膜离子电导增加。ADP使细胞膜去极化，其作用比ATP弱。AMP和腺苷均使细胞膜超极化。结果提供了证据，表明在兔耳动脉中，e.j.p.可被ATP模拟。然而，只有当ATP随着连续的神经放电以增加的量释放时，它才能解释快速e.j.p.。报道的ATP受体阻断剂在此组织中并未阻断对ATP的反应。
