Influence of altering cellular magnesium content on vascular smooth muscle contractility.
Influence of altering cellular magnesium content on vascular smooth muscle contractility.
复制标题
改变细胞镁含量对血管平滑肌收缩力的影响。
DOI：
10.1152/ajpcell.1986.251.5.c687
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Driska,SP
中科院分区：
文献类型：
--
作者：
Ford,GD;Driska,SP
在含有不同量 MgCl2（0、0.6、1.2、3、5、10 和 15 mM）的高 K+、无 Ca2+ 溶液中孵育 4 小时，猪颈动脉条中的组织和细胞 Mg 水平发生变化。孵育后立即测定总镁含量，称为组织镁含量，并在重新暴露于含有 1.2 mM Mg2+ 的正常生理盐溶液 (PSS) 后 1 小时和 3 小时测定。根据该数据计算细胞镁水平。孵育后组织 Mg 立即发生深刻变化，值范围从 7.3 mumol/g 干重到 71.4 mumol/g 干重，但仅在那些在 15 mM Mg2+ 中孵育的条带中，在重新暴露于正常 PSS 后仍显着升高。然而，如果孵育溶液和孵育后溶液中均包含 1 微摩尔哇巴因，则计算出的细胞镁水平仍然显着升高。经过相同 4 小时孵育程序的组织中对高 K+ 的反应表现出与细胞镁水平相同的模式。无论是否存在外部 Ca2+，孵育后对去甲肾上腺素反应的变化取决于去甲肾上腺素的剂量和孵育介质中 Mg2+ 的水平。看来肌浆镁水平能够通过影响收缩蛋白水平和激活剂 Ca2+ 的输送来调节动脉收缩力。
Tissue and cellular Mg levels in porcine carotid arterial strips were varied by 4-h incubation in high-K+, Ca2+-free solutions containing variable amounts of MgCl2 (0, 0.6, 1.2, 3, 5, 10, and 15 mM). The total Mg content, designated tissue Mg, was determined immediately after the incubation and also 1 and 3 h after reexposure to a normal physiological salt solution (PSS) containing 1.2 mM Mg2+. Cellular Mg levels were calculated from this data. The tissue Mg was profoundly altered immediately following the incubation, with values ranging from 7.3 mumol/g dry wt to 71.4 mumol/g dry wt, but remained significantly elevated following reexposure to normal PSS only in those strips incubated in 15 mM Mg2+. The calculated cellular Mg levels, however, did remain significantly elevated if 1 microM ouabain was included in both the incubation and post-incubation solutions. The response to high K+ in tissues subjected to the same 4-h incubation procedure exhibited the same pattern as the cellular Mg levels. Postincubation changes in the response to norepinephrine, either in the presence or absence of external Ca2+, depended on both the dose of norepinephrine and the level of Mg2+ in the incubation medium. It appears sarcoplasmic Mg levels are capable of modulating arterial contractility through influences at both the level of contractile proteins and the delivery of activator Ca2+.