Nakahata Katsutoshi, Kinoshita Hiroyuki, Tokinaga Yasuyuki, Ishida Yuko, Kimoto Yoshiki, Dojo Mayuko, Mizumoto Kazuhiro, Ogawa Koji, Hatano Yoshio
Department of Anesthesiology, Wakayama Medical University, Wakayama, Japan.
Anesth Analg. 2006 Feb;102(2):571-6. doi: 10.1213/01.ane.0000194303.00844.5e.
Although inward rectifier K+ channels contribute to the regulation of cerebral circulation, dilation of cerebral microvasculature mediated by these channels has not been demonstrated in chronic hypertension. We designed the present study to examine the roles of inward rectifier K+ channels in the vasodilation produced by increased levels of extracellular K+ in cerebral parenchymal arterioles from hypertensive and normotensive rats. During constriction to prostaglandin F2alpha (5 x 10(-7) M), the arterioles within brain slices were evaluated using computer-assisted microscopy. Potassium chloride (KCl) induced vasodilation in cerebral arterioles from normotensive (5-10 mM) and hypertensive (5-15 mM) rats, whereas an inward rectifier K+ channel antagonist barium chloride (BaCl2; 10(-5) M) completely abolished the vasodilation in both strains. In arterioles of hypertensive rats, vasodilator responses to KCl were augmented compared with those in normotensive rats. In contrast, the vasodilator responses induced by sodium nitroprusside (3 x 10(-8) to 3 x 10(-6) M) in these two strains were similar. These results suggest that in cerebral cortex parenchymal microvessels, inward rectifier K+ channels play a crucial role in vasodilation produced by extracellular K+ and that the dilation of cerebral arterioles via these channels is augmented in chronic hypertension.
尽管内向整流钾通道有助于调节脑循环，但在慢性高血压中，由这些通道介导的脑微血管扩张尚未得到证实。我们设计了本研究，以检验内向整流钾通道在高血压和正常血压大鼠脑实质小动脉中细胞外钾水平升高所产生的血管舒张中的作用。在对前列腺素F2α（5×10⁻⁷ M）产生收缩反应期间，使用计算机辅助显微镜评估脑切片内的小动脉。氯化钾（KCl）可诱导正常血压（5 - 10 mM）和高血压（5 - 15 mM）大鼠脑小动脉的血管舒张，而内向整流钾通道拮抗剂氯化钡（BaCl₂；10⁻⁵ M）完全消除了两种品系的血管舒张。在高血压大鼠的小动脉中，与正常血压大鼠相比，对KCl的血管舒张反应增强。相反，硝普钠（3×10⁻⁸至3×10⁻⁶ M）在这两种品系中诱导的血管舒张反应相似。这些结果表明，在大脑皮质实质微血管中，内向整流钾通道在细胞外钾产生的血管舒张中起关键作用，并且在慢性高血压中，通过这些通道的脑小动脉扩张增强。
