Ca dependence of Na influx during treatment of rabbit aorta with NE and high K solutions.
Ca dependence of Na influx during treatment of rabbit aorta with NE and high K solutions.
复制标题
用 NE 和高 K 溶液处理兔主动脉期间 Na 流入的 Ca 依赖性。
DOI：
10.1152/ajpcell.1988.254.1.c75
复制
发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Jones,AW
中科院分区：
文献类型：
--
作者：
Aaronson,PI;Jones,AW
在用10 μ M去甲肾上腺素（NE）刺激或用80 mM K溶液去极化过程中，使用脉冲标记，冷洗技术，在离体兔主动脉中测量24 Na的细胞内流。NE引起Na内流增加2 - 3倍;在去极化组织中也观察到较小但显著的增加。基础和NE诱导的通量在1分钟显着增加了20分钟的预孵育在含2 mM EGTA的无钙溶液中;升高[Mg]在该溶液中降低了这些影响。低Ca（30 μ m）和高Mg（10 mM）的组合可防止高K诱导的内流。钙激动剂BAY-K 8644可增加~（24）Na内流。钙拮抗剂地尔硫卓以浓度依赖性方式抑制去极化刺激的24 Na内流，但对NE反应的阻断效果较差。延长NE加无钙培养基中的预孵育时间，从30秒延长至15分钟，可降低内流反应和收缩。暴露于NE无钙溶液后，24 Na内流在持续缺乏钙的情况下冲洗NE后10分钟仍保持升高。第二次暴露于NE在那个时候并没有增加流入。我们建议，24 Na流入的一个组成部分，在兴奋过程中直接依赖于细胞内[Ca]的上升。[Ca]对代谢H+产生的间接影响以及随后的Na+-H+交换刺激的作用也可能是一个因素。
Cellular influx of 24Na was measured in isolated rabbit aorta during stimulation with 10 microM norepinephrine (NE) or depolarization with 80 mM K solution, using a pulse-labeling, cold-wash technique. NE caused a two- to threefold increase in Na influx; a smaller but significant increase was also observed in depolarized tissues. Basal and NE-induced fluxes at 1 min were significantly increased by a 20-min preincubation in a Ca-free solution containing 2 mM EGTA; elevation of [Mg] in this solution reduced these effects. The high K-induced influx was prevented by a combination of low Ca (30 microns) and elevated Mg (10 mM). The Ca agonist, BAY-K 8644, increased 24Na influx. The Ca antagonist, diltiazem, inhibited the depolarization-stimulated 24Na influx in a concentration-dependent manner, but was less effective in blocking the response to NE. Extension of the preincubation in NE plus Ca-free medium from 30 s to 15 min decreased the influx response and contraction. After exposure to NE in Ca-free solution, 24Na influx remained elevated 10 min after washing out NE in the continued absence of Ca. A second exposure to NE at that time did not increase influx. We propose that a component of 24Na influx during excitation depends directly on a rise in intracellular [Ca]. The role of an indirect effect of [Ca] on metabolic H+ production with subsequent stimulation of the Na+-H+ exchange may also be a factor.