Asano M, Masuzawa-Ito K, Matsuda T, Suzuki Y, Oyama H, Shibuya M, Sugita K
Department of Pharmacology, Nagoya City University Medical School, Japan.
J Auton Nerv Syst. 1994 Sep;49 Suppl:S151-5. doi: 10.1016/0165-1838(94)90104-x.
To determine the possible role of Ca(2+)-activated K+ (KCa) channels in the regulation of resting tone of cerebral arteries, the effect of agents which interact with these channels on tension and 86Rb efflux was examined in endothelium-denuded strips of dog basilar artery, and data were compared with findings in the mesenteric artery. The basilar artery maintained a myogenic tone; that is, the resting tone decreased when nifedipine was added. The addition of charybdotoxin, a blocker of large conductance KCa channels, caused a concentration-dependent contraction in the basilar artery but not in the mesenteric artery. In strips preloaded with 86Rb, the basal 86Rb efflux rate constant was significantly greater in the basilar artery than in the mesenteric artery. Nifedipine decreased the basal 86Rb efflux rate constant only in the basilar artery. The basal 45Ca influx in the resting state of the basilar artery was significantly increased when compared with the mesenteric artery and this increase in the basilar artery was reduced by nifedipine. The results suggest that the charybdotoxin-sensitive KCa channels regulate the myogenic tone in the resting state of the basilar artery. The activation of KCa channels in the basilar artery appears to be secondary to the increased transmembrane Ca2+ influx probably via the activation of L-type voltage-dependent Ca2+ channels in the resting state of this artery.
为了确定钙激活钾（KCa）通道在调节脑动脉静息张力中的可能作用，研究了与这些通道相互作用的药物对狗基底动脉去内皮条带张力和⁸⁶Rb外流的影响，并将数据与肠系膜动脉的研究结果进行了比较。基底动脉维持肌源性张力；也就是说，加入硝苯地平后静息张力降低。加入大电导KCa通道阻滞剂蝎毒素，可引起基底动脉浓度依赖性收缩，但对肠系膜动脉无此作用。在预先加载⁸⁶Rb的条带中，基底动脉的基础⁸⁶Rb外流速率常数显著高于肠系膜动脉。硝苯地平仅降低基底动脉的基础⁸⁶Rb外流速率常数。与肠系膜动脉相比，基底动脉静息状态下的基础⁴⁵Ca内流显著增加，硝苯地平可降低基底动脉的这种增加。结果表明，蝎毒素敏感的KCa通道调节基底动脉静息状态下的肌源性张力。基底动脉中KCa通道的激活似乎继发于跨膜Ca²⁺内流的增加，这可能是通过该动脉静息状态下L型电压依赖性Ca²⁺通道的激活实现的。
