PRESSURE-DEPENDENT MEMBRANE DEPOLARIZATION IN CAT MIDDLE CEREBRAL-ARTERY
PRESSURE-DEPENDENT MEMBRANE DEPOLARIZATION IN CAT MIDDLE CEREBRAL-ARTERY
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DOI：
10.1161/01.res.55.2.197
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发表时间：
1984-01-01
影响因子：
20.1
通讯作者：
HARDER, DR
中科院分区：
文献类型：
--
作者：
HARDER, DR
研究了增加跨壁压对猫大脑中动脉肌膜电特性的影响。从猫脑中取出大脑中动脉，插管并进行准备，以便可以操纵节段内的跨壁压力。在不同的跨壁压力下用玻璃微电极记录细胞内膜电位。细胞内膜电位的变化与跨壁压的关系呈正斜率，相关系数为 0.79。用河豚毒素阻断神经兴奋和用酚妥拉明抑制α-肾上腺素能受体不仅没有阻断压力诱导的去极化，而且增加了细胞内膜电位与压力关系的斜率。当细胞外 Ca 浓度从 2.5-4.0 mM 升高时，该斜率增加；当细胞外 Ca 浓度降低至 0.5 mM 时，该斜率显着降低。当动脉制剂在加压前平衡于 0 mm Hg 时，仅在压力最初升高时记录动作电位，而在压力平台期间记录持续去极化。当动脉在 100 mm Hg 的跨壁压力下平衡 90 分钟时，记录自发动作电位，其频率随着压力的函数而增加，直到在高跨壁压力下细胞内膜电位接近 -30 mV 时它们失活。显微照片表明，这些容器在加压时要么保持直径，要么减小直径。这些发现提供了脑动脉直径的肌源性调节的细胞机制。
The effect of increasing transmural pressure on membrane electrical properties of cat middle cerebral arterial muscle was studied. Middle cerebral arteries were removed from the cat brain, cannulated, and prepared so that transmural pressure within a segment could be manipulated. Intracellular membrane potential was recorded with glass microelectrodes at various transmural pressures. There was a positive slope relating changes in intracellular membrane potential as a function of transmural pressure with a correlation coefficient of 0.79. Blockade of nerve excitation with tetrodotoxin and inhibition of .alpha.-adrenergic receptors with phenotolamine not only did not block the pressure-induced depolarization, but increased the slope of the intracellular membrane potential vs. pressure relationship. This slope was increased upon elevation of extracellular Ca concentration from 2.5-4.0 mM and was significantly reduced upon reduction of extracellular Ca concentration to 0.5 mM. When arterial preparations were equilibrated at 0 mm Hg prior to pressurization, action potentials were recorded only when pressure was initially elevated, while a sustained depolarization was recorded during the pressure plateau. When arteries were equilibrated at a transmural pressure of 100 mm Hg for 90 min, spontaneous action potentials were recorded which increased in frequency as a function of pressure until they were inactivated when intracellular membrane potential approached -30 mV at high transmural pressures. Photomicrographs demonstrated that these vessels either maintained or decreased diameter upon pressurization. These findings provide a cellular mechanism for myogenic regulation of cerebral arterial diameter.