Makita Y
Br J Pharmacol. 1983 Dec;80(4):671-9. doi: 10.1111/j.1476-5381.1983.tb10057.x.
In the guinea-pig renal artery and vein, the membrane potential was -66.8 mV and -46.8 mV, the length constant 0.54 mm and 0.43 mm, and the time constant 240 ms and 98 ms, respectively. The maximum slope of the depolarization produced by a 10 fold increase [K]o was 46 mV in the renal artery and 39 mV in the renal vein. Noradrenaline (NA over 5 X 10(-7)M in the artery and over 10(-7)M in the vein) depolarized the membrane and slightly reduced the membrane resistance, assessed from relative changes in the amplitude of electrotonic potential. The action of NA was suppressed by prazosin in the artery but by yohimbine in the vein, i.e. the alpha 1-adrenoceptor is present in the extrajunctional muscle membrane in the renal artery while the alpha 2-adrenoceptor is present in the renal vein. Dopamine and isoprenaline did not modify the membrane properties. In the renal artery, repetitive perivascular nerve stimulation (0.1 ms, 50 Hz, 5 shocks) evoked excitatory junction potential (e.j.p.). Applications of guanethidine (10(-6) M) or tetrodotoxin (3 X 10(-7) M) abolished the generation of the e.j.p.. Low concentrations of phentolamine (5 X 10(-7) M), prazosin (10(-7) M) and yohimbine (5 X 10(-7) M) enhanced the e.j.p. amplitude, while high concentrations of phentolamine (10(-5) M) and prazosin (greater than 10(-5) M) reduced the amplitude of e.j.p.s. NA, dopamine and clonidine consistently suppressed the amplitude of e.j.ps, at any given concentration over 10(-7) M. Spontaneous generated miniature e.j.ps (m.e.j.ps) were recorded on rare occasions. Phentolamine and yohimbine both at 5 x 10(-7) M and prazosin 10(-7) M increased the appearance of m.e.j.ps. 5 In the renal vein, repetitive nerve stimulation failed to generate the e.j.p. Sympathetic innervation to this tissue seems to be sparse. 6 Specificity of innervation and adrenoceptors present on smooth muscle cells in both the renal artery and vein are discussed, and the presynaptic regulation ofNA release is compared with findings in other vascular tissues.
在豚鼠肾动脉和肾静脉中，膜电位分别为-66.8 mV和-46.8 mV，长度常数分别为0.54 mm和0.43 mm，时间常数分别为240 ms和98 ms。细胞外钾离子浓度([K]o)增加10倍所产生的去极化的最大斜率，在肾动脉中为46 mV，在肾静脉中为39 mV。去甲肾上腺素（在动脉中浓度超过5×10⁻⁷M，在静脉中浓度超过10⁻⁷M）使膜去极化，并从电紧张电位幅度的相对变化评估得出，使膜电阻略有降低。动脉中哌唑嗪抑制去甲肾上腺素的作用，而静脉中育亨宾抑制其作用，即肾动脉的结外肌膜中存在α₁ - 肾上腺素能受体，而肾静脉中存在α₂ - 肾上腺素能受体。多巴胺和异丙肾上腺素不改变膜特性。在肾动脉中，重复的血管周围神经刺激（0.1 ms，50 Hz，5次电击）诱发兴奋性接头电位（e.j.p.）。应用胍乙啶（10⁻⁶ M）或河豚毒素（3×10⁻⁷ M）可消除e.j.p.的产生。低浓度的酚妥拉明（5×10⁻⁷ M）、哌唑嗪（10⁻⁷ M）和育亨宾（5×10⁻⁷ M）可增强e.j.p.的幅度，而高浓度的酚妥拉明（10⁻⁵ M）和哌唑嗪（大于10⁻⁵ M）则降低e.j.p.的幅度。在任何给定浓度超过10⁻⁷ M时，去甲肾上腺素、多巴胺和可乐定始终抑制e.j.p.的幅度。偶尔记录到自发产生的微小e.j.p.（m.e.j.p.）。5×10⁻⁷ M的酚妥拉明和育亨宾以及10⁻⁷ M的哌唑嗪均增加了m.e.j.p.的出现频率。在肾静脉中，重复神经刺激未能产生e.j.p.。该组织的交感神经支配似乎很稀疏。6讨论了肾动脉和肾静脉平滑肌细胞上神经支配和肾上腺素能受体的特异性，并将去甲肾上腺素释放的突触前调节与其他血管组织的研究结果进行了比较。
