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去甲肾上腺素引起基底动脉收缩和软脑膜动脉扩张的膜电机制。

Membrane electrical mechanism of basilar artery constriction and pial artery dilation by norepinephrine.

作者信息

Harder D R, Abel P W, Hermsmeyer K

出版信息

Circ Res. 1981 Dec;49(6):1237-42. doi: 10.1161/01.res.49.6.1237.

Abstract

To study the mechanism by which norepinephrine acts on vascular muscle cell membrane, we recorded membrane potential with intracellular microelectrodes in isolated cat basilar and pial arteries. On addition of norepinephrine concentrations less than 1 microM, pial arteries hyperpolarized and relaxed while basilar arteries depolarized and contracted. Relaxation and hyperpolarization of the pial arteries occurred without the need for addition of any other drug, which indicates the relaxation of spontaneous tone. The relaxation and hyperpolarization could be completely blocked by addition of propranolol before exposure to norepinephrine. The depolarization and contraction of both basilar and pial arteries was blocked by the previous exposure to phentolamine. Electrical spikes were not found spontaneously, but could be induced in both arteries by tetraethylammonium and subsequent addition of norepinephrine, blockable by phentolamine. We conclude that membrane property differences between basilar and pial arteries result in qualitatively different effects of norepinephrine.

摘要

为了研究去甲肾上腺素作用于血管肌细胞膜的机制,我们用细胞内微电极记录了分离的猫基底动脉和软脑膜动脉的膜电位。加入浓度低于1微摩尔的去甲肾上腺素后,软脑膜动脉超极化并舒张,而基底动脉去极化并收缩。软脑膜动脉的舒张和超极化无需添加任何其他药物即可发生,这表明是自发张力的舒张。在暴露于去甲肾上腺素之前加入普萘洛尔可完全阻断舒张和超极化。基底动脉和软脑膜动脉的去极化和收缩可被预先暴露于酚妥拉明所阻断。未自发发现电尖峰,但在两条动脉中均可由四乙铵诱导,随后加入去甲肾上腺素,可被酚妥拉明阻断。我们得出结论,基底动脉和软脑膜动脉之间的膜特性差异导致去甲肾上腺素产生质的不同的效应。

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