Linnik M D, Lee T J
Southern Illinois University School of Medicine, Department of Pharmacology, Springfield 62708.
J Cereb Blood Flow Metab. 1989 Apr;9(2):219-25. doi: 10.1038/jcbfm.1989.32.
Electrically stimulated neurogenic vasodilation and endothelial-dependent cholinergic vasodilation in cerebral arteries are both blocked by hemoglobin. To determine if neurogenic vasodilation has a cholinergic component, we examined the effect of hemoglobin on neurogenic responses and perivascular cholinergic parameters in isolated porcine cerebral arteries. The perfused circle of Willis has a mixed response to transmural nerve stimulation (TNS) that is predominantly vasodilation. Exposure to hemoglobin (5 microM) causes constriction of this preparation while simultaneously blocking TNS-induced vasodilation. At similar concentrations, however, hemoglobin did not alter electrically stimulated, tetrodotoxin-sensitive release of acetylcholine. Hemoglobin also had no effect on neuronal choline uptake or esteratic inactivation of acetylcholine. These results demonstrate the ability of low concentrations of hemoglobin to alter cerebral neurogenic vasodilation. The failure of hemoglobin to affect any aspect of cholinergic transmission, however, provides further evidence against a direct vasodilatory role for acetylcholine as a terminal transmitter in isolated cerebral blood vessels.
脑动脉中电刺激引起的神经源性血管舒张和内皮依赖性胆碱能血管舒张均被血红蛋白阻断。为了确定神经源性血管舒张是否具有胆碱能成分，我们研究了血红蛋白对离体猪脑动脉神经源性反应和血管周围胆碱能参数的影响。灌注的 Willis 环对跨壁神经刺激（TNS）有混合反应，主要是血管舒张。暴露于血红蛋白（5 microM）会导致该制剂收缩，同时阻断 TNS 诱导的血管舒张。然而，在相似浓度下，血红蛋白并未改变电刺激引起的、对河豚毒素敏感的乙酰胆碱释放。血红蛋白对神经元胆碱摄取或乙酰胆碱的酯解失活也没有影响。这些结果证明了低浓度血红蛋白改变脑源性神经血管舒张的能力。然而，血红蛋白未能影响胆碱能传递的任何方面，这进一步证明乙酰胆碱在离体脑血管中作为终末递质不具有直接的血管舒张作用。
