Ohhashi T, Azuma T
Microvasc Res. 1986 Jan;31(1):31-40. doi: 10.1016/0026-2862(86)90004-x.
We studied isolated bovine mesenteric lymphatics to elucidate the pharmacological characteristics of pre- and postjunctional alpha-adrenoceptors at the sympathetic neuroeffector junction. Cylindrical strips were incubated with [3H]-noradrenaline and mounted for superfusion. Electrical stimulation (2 Hz, 0.5 msec, 50 V) augmented the fractional release of labeled noradrenaline. Exogenous noradrenaline and clonidine caused a depression of the evoked tracer release. Phenoxybenzamine and yohimbine markedly enhanced the evoked overflow of adrenergic transmitter. Rings of lymphatic vessels were mounted for isometric tension recording in organ chambers filled with Krebs-Ringer bicarbonate solution. The vessels contracted when exposed to phenylephrine and clonidine. The ED50 of clonidine was significantly lower than that of phenylephrine. Prazosin caused a parallel shift to the right of the dose-response curve to phenylephrine. The antagonist, however, suppressed the magnitude of the maximum response to clonidine. Yohimbine caused parallel shift to the right of the dose-response curves to phenylephrine and clonidine, respectively. The Schild plots for yohimbine demonstrated that the drug was a competitive antagonist to phenylephrine and clonidine. The pA2 value of yohimbine to clonidine (7.6 +/- 0.4) was larger than that to phenylephrine (6.2 +/- 0.4). The pA2 value of prazosin to phenylephrine was 7.2 +/- 0.3. These results suggest that prejunctional alpha-adrenoceptors are involved in the negative feedback mechanism for autoregulation of noradrenaline release during postganglionic sympathetic nerve stimulation, and that both alpha 1- and alpha 2-like adrenoceptors do exist on lymphatic smooth muscle cells.
我们研究了分离的牛肠系膜淋巴管，以阐明交感神经效应器接头处节前和节后α-肾上腺素能受体的药理学特性。将圆柱形条带与[3H]-去甲肾上腺素一起孵育，然后安装用于灌注。电刺激（2Hz，0.5毫秒，50V）增加了标记去甲肾上腺素的分数释放。外源性去甲肾上腺素和可乐定导致诱发的示踪剂释放减少。酚苄明和育亨宾显著增强了肾上腺素能递质的诱发溢出。将淋巴管环安装在充满 Krebs-Ringer 碳酸氢盐溶液的器官浴槽中进行等长张力记录。当暴露于去氧肾上腺素和可乐定时，血管收缩。可乐定的半数有效剂量（ED50）显著低于去氧肾上腺素。哌唑嗪使去氧肾上腺素的剂量-反应曲线向右平行移动。然而，该拮抗剂抑制了对可乐定的最大反应幅度。育亨宾分别使去氧肾上腺素和可乐定的剂量-反应曲线向右平行移动。育亨宾的 Schild 图表明该药物是去氧肾上腺素和可乐定的竞争性拮抗剂。育亨宾对可乐定的 pA2 值（7.6±0.4）大于对去氧肾上腺素的 pA2 值（6.2±0.4）。哌唑嗪对去氧肾上腺素的 pA2 值为 7.2±0.3。这些结果表明，节前α-肾上腺素能受体参与了节后交感神经刺激期间去甲肾上腺素释放的负反馈自动调节机制，并且淋巴管平滑肌细胞上确实存在α1-和α2-样肾上腺素能受体。
