Prior H M, Webster N, Quinn K, Beech D J, Yates M S
Department of Pharmacology, University of Leeds, UK.
Cardiovasc Res. 1998 Mar;37(3):780-90. doi: 10.1016/s0008-6363(97)00237-x.
To investigate the mechanism of K(+)-induced vasodilation in a small artery from the kidney, with a particular emphasis on the role of inward rectifier K+ channels.
Lumen diameter and isometric tension recordings have been made from rabbit renal arcuate artery using pressurised- and wire-myography respectively. In addition, conventional whole-cell and amphotericin-perforated patch whole-cell recordings have been made from single smooth muscle cells isolated from the vessel.
Arcuate arteries dilated when the extracellular K+ concentration was raised to 8-10 mM from either zero or a normal physiological level of about 6 mM. The effect was not endothelium-dependent. Application of 0.01-1 mM Ba2+ to block inward rectifier K+ channels had no significant effect on K(+)-induced vasodilation in the arcuate artery, but under the same experimental conditions K(+)-induced dilation of the rat posterior cerebral artery was abolished by Ba2+. In the presence of 60 mM extracellular K+, inward rectifier K(+)-current was detectable in some single smooth muscle cells isolated from arcuate arteries but on average the current density was low (-1.44 pA pF-1 at -60 mV). K(+)-induced vasodilation of the arcuate artery was abolished by 10 microM ouabain and the half-effective concentration of K+ which induced vasodilation was 0.9-1.5 mM.
The observations suggest that an increase in the extracellular K+ concentration (up to about 10 mM) dilates the rabbit renal arcuate artery and that the primary mechanism underlying the effect may be stimulation of Na(+)-K+ ATPase in the smooth muscle cell membrane. Inward rectifier K+ channels have a low average density in smooth muscle cells isolated from arcuate arteries and play no significant role in K(+)-induced vasodilation.
研究钾离子诱导肾小动脉血管舒张的机制，特别强调内向整流钾通道的作用。
分别使用压力肌动描记法和线肌动描记法记录兔肾弓状动脉的管腔直径和等长张力。此外，还对从该血管分离出的单个平滑肌细胞进行了传统的全细胞记录和两性霉素穿孔膜片全细胞记录。
当细胞外钾离子浓度从零或约6 mM的正常生理水平升高到8 - 10 mM时，弓状动脉扩张。该效应不依赖于内皮。应用0.01 - 1 mM的钡离子阻断内向整流钾通道，对钾离子诱导的弓状动脉血管舒张无显著影响，但在相同实验条件下，钡离子可消除钾离子诱导的大鼠大脑后动脉扩张。在细胞外钾离子浓度为60 mM时，在从弓状动脉分离出的一些单个平滑肌细胞中可检测到内向整流钾电流，但平均电流密度较低（在-60 mV时为-1.44 pA pF-1）。10 μM哇巴因可消除钾离子诱导的弓状动脉血管舒张，诱导血管舒张的钾离子半数有效浓度为0.9 - 1.5 mM。
这些观察结果表明，细胞外钾离子浓度升高（高达约10 mM）可使兔肾弓状动脉扩张，其作用的主要机制可能是刺激平滑肌细胞膜上的钠钾ATP酶。从弓状动脉分离出的平滑肌细胞中内向整流钾通道的平均密度较低，在钾离子诱导的血管舒张中不起重要作用。
