MEMBRANE HYPERPOLARIZATION IS A MECHANISM OF ENDOTHELIUM-DEPENDENT CEREBRAL VASODILATION
MEMBRANE HYPERPOLARIZATION IS A MECHANISM OF ENDOTHELIUM-DEPENDENT CEREBRAL VASODILATION
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DOI：
10.1152/ajpheart.1990.259.3.h668
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发表时间：
1990-09-01
影响因子：
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通讯作者：
BRAYDEN, JE
中科院分区：
文献类型：
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作者：
BRAYDEN, JE
乙酰胆碱（ACh）诱导的脑动脉超极化需要功能性内皮。钾通道阻滞剂可逆转超极化。本研究的目的是确定超极化是否与离体脑动脉的内皮依赖性舒张有因果关系。乙酰胆碱超极化兔大脑中动脉高达19 mV。在没有内皮细胞或存在钾通道抑制剂（3 × 104）的动脉中，超极化持续存在，并且不发生。10-6 M格列本脲或5 ×10-5 M BaCl 2）。ACh诱导的扩张反应被格列本脲或BaCl2抑制，但未被消除。亚甲蓝也抑制了扩张反应，格列本脲或BaCl 2和亚甲蓝的组合大大减少了扩张。一氧化氮放松，但不hyperplasia的血管平滑肌细胞，氯化钡对一氧化氮诱导的舒张没有影响。这些数据表明，整体脑动脉扩张剂对ACh的反应是由膜超极化的联合作用决定的，膜超极化关闭电压依赖性钙通道，以及第二种内皮因子的作用，可能是内皮衍生的舒张因子。
Actylcholine (ACh)-induced hyperpolarization of cerebral arteries requires a functional endothelium. The hyperpolarization is reversed by potassium-channel blockers. The goal of this study was to determine whether the hyperpolarization is causally related to endothelium-dependent dilation of isolated cerebral arteries. ACh hyperpolarized rabbit middle cerebral arteries by up to 19 mV. The hyperpolarizations were sustained and did not occur in arteries without endothelial cells or in the presence of potassium-channel inhibitors (3 .times. 10-6 M glibenclamide or 5 .times. 10-5 M BaCl2). ACh-induced dilator responses were inhibited but not abolished by glibenclamide or BaCl2. Methylene blue also inhibited the dilator responses, and a combination of glibenclamide or BaCl2 and methylene blue greatly diminished the dilation. Nitric oxide relaxed but did not hyperpolarize the vascular smooth muscle cells, and BaCl2 had no effect on the nitric oxide-induced relaxations. These data indicate that the overall cerebral arterial dilator response to ACh is determined by the combined effects of membrane hyperpolarization, which closes voltage-dependent calcium channels, and the actions of a second endothlial factor, probably endothelium derived relaxing factor.