Brayden J E, Large W A
Br J Pharmacol. 1986 Sep;89(1):163-71. doi: 10.1111/j.1476-5381.1986.tb11132.x.
The nature of neurogenic vasodilatation was investigated in isolated segments of rabbit lingual artery. In separate experiments membrane responses to nerve stimulation were studied by use of microelectrodes. In the presence of guanethidine to block constrictor responses and noradrenaline to induce tone, field stimulation with trains of pulses (8 Hz for 0.5 to 4 s) produced vasodilatation. Atropine (10(-6) M) reduced the relaxations to about 50% of the control values while the induced vasodilatations were potentiated by physostigmine. Tetrodotoxin (TTX, 10(-7) M) blocked all nerve-evoked responses. These data suggest that there is a cholinergic and a non-cholinergic component of the vasodilatation produced by nerve stimulation in the rabbit lingual artery. Single stimuli did not evoke electrophysiological responses. With parameters similar to those used in the mechanical studies, periarterial stimulation in the presence of guanethidine evoked membrane hyperpolarizations which achieved amplitudes of up to 11 mV. The ionophoretic application of acetylcholine (ACh) produced hyperpolarization. The inhibitory junction potentials (i.j.ps) but not the ionophoretic-induced responses were blocked by TTX. The nerve-evoked and the ACh-induced hyperpolarizations were potentiated by physostigmine (5 X 10(-7) M) and totally blocked by atropine (10(-7) M). I.j.ps and hyperpolarization to ionophoresis of ACh were recorded from arteries in which the endothelium had been removed by mechanical rubbing. Mechanical relaxation to field stimulation and ACh was observed in preparations without endothelium. These data suggest that the cholinergic component of the neurogenic vasodilatation in the rabbit lingual artery is accompanied by hyperpolarization. The non-cholinergic component does not appear to possess an electrophysiological correlate. In addition, it seems that the action of nerve-released ACh is mediated by muscarinic receptors which are situated directly on the vascular smooth muscle cells.
在兔舌动脉离体节段中研究了神经源性血管舒张的性质。在单独的实验中，使用微电极研究了对神经刺激的膜反应。在存在胍乙啶以阻断收缩反应和去甲肾上腺素以诱导张力的情况下，用脉冲串（8Hz，持续0.5至4秒）进行场刺激可产生血管舒张。阿托品（10⁻⁶M）使舒张反应降低至对照值的约50%，而毒扁豆碱可增强诱导的血管舒张。河豚毒素（TTX，10⁻⁷M）阻断所有神经诱发的反应。这些数据表明，兔舌动脉中神经刺激产生的血管舒张存在胆碱能和非胆碱能成分。单个刺激未诱发电生理反应。在与机械研究中使用的参数相似的情况下，在胍乙啶存在下进行动脉周围刺激可诱发膜超极化，其幅度可达11mV。乙酰胆碱（ACh）的离子电泳应用产生超极化。抑制性接头电位（i.j.ps）而非离子电泳诱导的反应被TTX阻断。毒扁豆碱（5×10⁻⁷M）可增强神经诱发的和ACh诱导的超极化，而阿托品（10⁻⁷M）可完全阻断。在通过机械摩擦去除内皮的动脉中记录到了i.j.ps和对ACh离子电泳的超极化。在无内皮的制剂中观察到对场刺激和ACh的机械舒张。这些数据表明，兔舌动脉中神经源性血管舒张的胆碱能成分伴随着超极化。非胆碱能成分似乎不具有电生理相关性。此外，似乎神经释放的ACh的作用是由直接位于血管平滑肌细胞上的毒蕈碱受体介导的。
