PRESSURE-INDUCED ACTIVATION OF MEMBRANE K+ CURRENT IN RAT SAPHENOUS ARTERY
PRESSURE-INDUCED ACTIVATION OF MEMBRANE K+ CURRENT IN RAT SAPHENOUS ARTERY
复制标题
DOI：
10.1161/01.hyp.19.6.725
复制
发表时间：
1992-06-01
期刊：
影响因子：
8.3
通讯作者：
RUSCH, NJ
中科院分区：
文献类型：
--
作者：
BERCZI, V;STEKIEL, WJ;RUSCH, NJ
孤立动脉的加压可能导致 Ca2+ 依赖性收缩和膜去极化。由于一些血管肌肉 K+ 通道的开放状态概率因胞质 Ca2+ 的增加和膜去极化而增加，因此我们研究了腔内压力的增加激活离体、灌注的大鼠隐动脉中 K+ 通道的可能性。管腔内压力从 5 毫米汞柱逐步增加到 205 毫米汞柱，导致动脉收缩增加，在生理盐溶液中测得的动脉收缩比在不含 Ca2+ 的溶液中更小。在生理盐溶液中添加 10 mM 四乙铵以阻断动脉肌肉 K+ 通道，在压力高于 25 mm Hg 时导致直径逐渐减小。膜电位的微电极测量表明，四乙铵在 105 mm Hg (16+/-1 mV) 下比在 25 mm Hg (10+/-1 mV) 下对动脉肌肉的去极化作用更大。 K+电流对四乙铵的敏感性也在来自同一动脉的膜片钳血管肌细胞中得到证实。 1 和 10 mM 四乙铵分别抑制全细胞 K+ 峰值电流 47% 和 79%。 Ca2+ 离子载体 A23187 (10-mu-M) 将相同的电流增强了 3.6 倍，表明存在 Ca2+ 依赖性。我们得出的结论是，腔内压力的增加逐渐激活动脉肌膜中四乙铵敏感的 K+ 通道。这可以作为一种负反馈机制来限制压力引起的动脉收缩。
Pressurization of isolated arteries may result in Ca2+-dependent contraction and membrane depolarization. Because the open state probability of some vascular muscle K+ channels is augmented by rises in cytosolic Ca2+ and membrane depolarization, we investigated the possibility that increases in intraluminal pressure activate K+ channels in isolated, perfused rat saphenous arteries. Stepwise increases in intraluminal pressure from 5 to 205 mm Hg resulted in increasing, active arterial contraction, measured as smaller diameters in physiological salt solution than in Ca2+-free solution. Addition of 10 mM tetraethylammonium to the physiological salt solution to block arterial muscle K+ channels caused progressively greater diameter reductions at pressures above 25 mm Hg. Microelectrode measurements of membrane potential showed that tetraethylammonium depolarized arterial muscle more at 105 mm Hg (16+/-1 mV) than at 25 mm Hg (10+/-1 mV). The sensitivity of K+ current to tetraethylammonium was also demonstrated in patch-clamped vascular muscle cells from the same arteries. Peak whole-cell K+ current was suppressed 47% and 79% by 1 and 10 mM tetraethylammonium, respectively. This same current was enhanced 3.6 -fold by the Ca2+ ionophore A23187 (10-mu-M), suggesting a Ca2+ dependence. We conclude that increases in intraluminal pressure progressively activate tetraethylammonium-sensitive K+ channels in the arterial muscle membrane. This can serve as a negative feedback mechanism to limit pressure-induced arterial constriction.