Kajiwara M, Kitamura K, Kuriyama H
J Physiol. 1981 Jun;315:283-302. doi: 10.1113/jphysiol.1981.sp013748.
Effects of noradrenaline and alpha-adrenoceptor blocking agents on neuromuscular transmission of the guinea-pig ear artery were assessed using the micro-electrode method.1. The mean membrane potential, and length and time constants of the longitudinally oriented muscle cells were -64.5 +/- 5 mV (n = 150), 1.03 +/- 0.16 mm (n = 15) and 410 +/- 40 msec (n = 7) respectively. From the current-voltage relationship, weak outward current pulses produced an anomalous rectification of the membrane while stronger intensities produced a normal rectification of the membrane with a depolarization over 10-15 mV.2. Brief stimulation (0.1-0.5 msec) of the tissue produced an excitatory junction potential (e.j.p.). Facilitation produced by repetitive stimulation was evident only on very rare occasions. Higher stimulus intensities caused a stepwise increase of the amplitude of e.j.p.s.3. Spontaneously generated miniature excitatory junction potentials (m.e.j.p.s) were recorded from the muscle membrane. In many cells, the interval and amplitude histograms of m.e.j.p.s showed skew curves. On rare occasions, a bell-shaped amplitude distribution (quantal release of packeted noradrenaline (NA)) was observed.4. NA (> 3 x 10(-7)m) depolarized the membrane and increased the membrane resistance, as measured from the amplitude of the electrotonic potential. Phentolamine suppressed the NA-induced depolarization. However, high concentrations of phentolamine (> 10(-5)m) depolarized the membrane and increased the membrane resistance.5. NA (10(-8)m) caused no change in membrane potential though it suppressed the amplitude of an e.j.p. produced by a single stimulus, but did not suppress the amplitude of the subsequent e.j.p.s evoked by repetitive stimulation (0.2-2.0 Hz). A higher concentration of NA (3 x 10(-7)m) depolarized the membrane and markedly suppressed the amplitude of e.j.p.s. On the other hand, NA (10(-8) or 2 x 10(-8)m) generated burst discharges of m.e.j.p.s between silent periods or random generation.6. Phentolamine (10(-6)m) markedly enhanced the amplitude of e.j.p.s and caused a smooth facilitation in response to a train of stimuli with no effect on the membrane potential. A stepwise change in the amplitude of e.j.p.s was no longer observed at any given stimulus frequency and intensity.7. Phenoxybenzamine (10(-7)m) suppressed the amplitude of e.j.p.s with no change in the membrane potential.8. The results led to the conclusion that, at a concentration which has no effect on the post-junctional muscle membrane, NA and phentolamine seemed to be more effective on prejunctional adrenoceptors, while phenoxybenzamine seemed to have a greater effect on post-junctional adrenoceptors. NA depresses adrenergic transmission by negative feed-back, while the enhancing action of phentolamine can be explained partly by blocking of prejunctional adrenoceptors and, in addition, by an increase of NA release.
采用微电极法评估去甲肾上腺素和α-肾上腺素能受体阻断剂对豚鼠耳动脉神经肌肉传递的影响。1. 纵向排列的肌细胞的平均膜电位、长度和时间常数分别为-64.5±5 mV（n = 150）、1.03±0.16 mm（n = 15）和410±40毫秒（n = 7）。根据电流-电压关系，弱外向电流脉冲使膜产生反常整流，而较强强度则使膜产生正常整流，伴有超过10 - 15 mV的去极化。2. 对组织进行短暂刺激（0.1 - 0.5毫秒）可产生兴奋性接头电位（e.j.p.）。重复刺激产生的易化仅在极少数情况下明显。较高的刺激强度导致e.j.p.的幅度呈阶梯式增加。3. 从肌膜记录到自发产生的微小兴奋性接头电位（m.e.j.p.）。在许多细胞中，m.e.j.p.的间隔和幅度直方图显示为偏态曲线。在极少数情况下，观察到钟形幅度分布（成包去甲肾上腺素（NA）的量子释放）。4. NA（>3×10⁻⁷m）使膜去极化并增加膜电阻，这是根据电紧张电位的幅度测量的。酚妥拉明抑制NA诱导的去极化。然而，高浓度的酚妥拉明（>10⁻⁵m）使膜去极化并增加膜电阻。5. NA（10⁻⁸m）虽抑制单个刺激产生的e.j.p.的幅度，但对膜电位无影响，且不抑制重复刺激（0.2 - 2.0 Hz）诱发的后续e.j.p.的幅度。较高浓度的NA（3×10⁻⁷m）使膜去极化并显著抑制e.j.p.的幅度。另一方面，NA（10⁻⁸或2×10⁻⁸m）在静息期之间产生m.e.j.p.的爆发性放电或随机产生。6. 酚妥拉明（10⁻⁶m）显著增强e.j.p.的幅度，并在对一串刺激的反应中产生平滑的易化，对膜电位无影响。在任何给定的刺激频率和强度下，不再观察到e.j.p.幅度的阶梯式变化。7. 酚苄明（10⁻⁷m）抑制e.j.p.的幅度，膜电位无变化。8. 结果得出结论，在对突触后肌膜无影响的浓度下，NA和酚妥拉明似乎对突触前肾上腺素能受体更有效，而酚苄明似乎对突触后肾上腺素能受体有更大影响。NA通过负反馈抑制肾上腺素能传递，而酚妥拉明的增强作用部分可通过阻断突触前肾上腺素能受体以及此外通过增加NA释放来解释。
