Horiuchi Tetsuyoshi, Dietrich Hans H, Hongo Kazuhiro, Dacey Ralph G
Department of Neurosurgery, Washington University School of Medicine, St Louis, Mo 63110, USA.
Stroke. 2002 Nov;33(11):2692-9. doi: 10.1161/01.str.0000034791.52151.6b.
Extracellular concentration of potassium ion ([K+]o) may have a significant influence on the cerebral circulation in health and disease. Mechanisms of [K+]o-induced conducted vasomotor responses in cerebral arterioles, possibly linking microvascular regulation to neuronal activity, have not been examined.
We analyzed vascular responses to small increases of [K+]o (up to 5 mmol/L) in isolated, cannulated, and pressurized rat cerebral arterioles (36.5+/-1.4 micro m). [K+]o was elevated globally through extraluminal application or locally through micropipette, while arteriolar diameter was measured online.
Elevation of [K+]o (5 mmol/L) produced dilation that was inhibited by ouabain but not BaCl2. Locally applied [K+]o (3 to 5 mmol/L) produced a biphasic response (initial constriction followed by dilation), both of which were conducted to the remote site (distance 1142+/-68 microm). Endothelial impairment inhibited conducted but not local biphasic responses. Extraluminal ouabain attenuated local and conducted secondary dilation but not initial constriction. The local biphasic response was unaffected by extraluminal or intraluminal BaCl2. Extraluminal but not intraluminal BaCl2 impaired both conducted constriction and dilation.
In rat penetrating arteriole, (1) [K+]o (3 to 5 mmol/L) strongly regulates arteriolar tone and causes conducted vasomotor responses; (2) local responses to elevated [K+]o are endothelium independent but conducted responses are dependent on an intact endothelium; (3) smooth muscle Na+-K+-ATPase activation is the generator of conducted dilation; and (4) smooth muscle inward rectifier potassium channels sustain conduction. Our findings suggest that potassium-induced conducted vasomotor responses may link local neuronal activity to microvascular regulation, which may be attenuated in pathological conditions.
钾离子细胞外浓度（[K+]o）可能对健康及疾病状态下的脑循环产生显著影响。目前尚未研究[K+]o诱导脑小动脉传导性血管舒缩反应的机制，而这一机制可能将微血管调节与神经元活动联系起来。
我们分析了分离、插管并加压的大鼠脑小动脉（36.5±1.4微米）对[K+]o小幅升高（高达5毫摩尔/升）的血管反应。通过管腔外应用使[K+]o整体升高，或通过微量移液器局部升高，同时在线测量小动脉直径。
[K+]o升高至5毫摩尔/升会产生舒张反应，该反应可被哇巴因抑制，但不受氯化钡抑制。局部应用[K+]o（3至5毫摩尔/升）会产生双相反应（先收缩后舒张），这两种反应都会传导至远处部位（距离为1142±68微米）。内皮损伤会抑制传导性反应，但不影响局部双相反应。管腔外哇巴因会减弱局部和传导性的继发性舒张反应，但不影响初始收缩反应。局部双相反应不受管腔外或管腔内氯化钡的影响。管腔外而非管腔内的氯化钡会损害传导性收缩和舒张反应。
在大鼠穿通动脉中，（1）[K+]o（3至5毫摩尔/升）强烈调节小动脉张力并引起传导性血管舒缩反应；（2）对升高的[K+]o的局部反应不依赖内皮，但传导性反应依赖完整的内皮；（3）平滑肌钠钾ATP酶激活是传导性舒张的产生机制；（4）平滑肌内向整流钾通道维持传导。我们的研究结果表明，钾诱导的传导性血管舒缩反应可能将局部神经元活动与微血管调节联系起来，而在病理状态下这种联系可能会减弱。
