Harder D R
Circ Res. 1984 Aug;55(2):197-202. doi: 10.1161/01.res.55.2.197.
This study was undertaken to examine the effect of increasing transmural pressure on membrane electrical properties of cat middle cerebral arterial muscle. 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 phentolamine 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 calcium concentration from 2.5 to 4.0 mM and was significantly reduced upon reduction of extracellular calcium 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. However, when arteries were equilibrated at a transmural pressure of 100 mm Hg for 90 minutes, 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.
本研究旨在探讨增加跨壁压力对猫大脑中动脉肌肉膜电特性的影响。从猫脑中取出大脑中动脉,插管并进行处理,以便能够控制节段内的跨壁压力。在不同的跨壁压力下,用玻璃微电极记录细胞内膜电位。细胞内膜电位变化与跨壁压力之间呈正斜率关系,相关系数为0.79。用河豚毒素阻断神经兴奋以及用酚妥拉明抑制α-肾上腺素能受体,不仅没有阻断压力诱导的去极化,反而增加了细胞内膜电位与压力关系的斜率。当细胞外钙浓度从2.5 mM升高到4.0 mM时,该斜率增加;当细胞外钙浓度降低到0.5 mM时,该斜率显著降低。当动脉标本在加压前平衡于0 mmHg时,仅在压力最初升高时记录到动作电位,而在压力平台期记录到持续的去极化。然而,当动脉在100 mmHg的跨壁压力下平衡90分钟时,记录到自发动作电位,其频率随压力增加,直到在高跨壁压力下细胞内膜电位接近-30 mV时失活。显微照片显示,这些血管在加压时要么保持直径不变,要么直径减小。这些发现为脑动脉直径的肌源性调节提供了一种细胞机制。