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首页> 外文期刊>American Journal of Physiology >Abnormal platelet Ca2+ handling accompanied by increased cytosolic free Mg2+ in essential hypertension.
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Abnormal platelet Ca2+ handling accompanied by increased cytosolic free Mg2+ in essential hypertension.

机译：原发性高血压患者血小板Ca2 +异常处理并伴有胞浆游离Mg2 +增加。

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摘要

To test the hypothesis that abnormal platelet Ca2+ handling in essential hypertension results from cellular Mg2+ deficiency, cytosolic free Mg2+ concentration ([Mg2+]i) and Ca2+ metabolism were studied in mag-fura 2 and fura 2-loaded platelets from 30 essential hypertensive patients and 30 sex- and age-matched normotensive controls. Basal cytosolic free Ca2+ concentration ([Ca2+]i) and intracellular Ca2+ discharge capacity were higher in hypertensives than in normotensives (22 +/- 5 vs. 18 +/- 5 nM, P < 0.05; 743 +/- 250 vs. 624 +/- 144 nM, P < 0.05, respectively). The thrombin (0. 03-1.0 U/ml)-evoked [Ca2+]i response was also enhanced in platelets from hypertensives in both the absence and presence of extracellular Ca2+. However, basal [Mg2+]i was higher in hypertensives than in normotensives (437 +/- 110 vs. 353 +/- 85 microM, P < 0.05), whereas serum Mg2+ was similar in the two groups. These results oppose the Mg2+ deficiency hypothesis in platelets in essential hypertension.
机译：为了验证以下假设，即原发性高血压中血小板Ca2 +的异常处理是由细胞Mg2 +缺乏引起的，研究了30名原发性高血压患者的mag-fura 2和呋喃2加载的血小板中无胞质Mg2 +浓度（[Mg2 +] i）和Ca2 +代谢30个按性别和年龄匹配的血压正常对照。高血压患者的基础细胞游离钙离子浓度（[Ca2 +] i）和细胞内Ca2 +排出量高于血压正常者（22 +/- 5 vs. 18 +/- 5 nM，P <0.05; 743 +/- 250 vs. 624分别为+/- 144 nM，P <0.05）。在不存在和存在细胞外Ca 2+的情况下，由高血压引起的血小板中凝血酶（0. 03-1.0 U / ml）引起的[Ca 2+] i反应也得到增强。然而，高血压患者的基础[Mg2 +] i高于正常血压（437 +/- 110 vs. 353 +/- 85 microM，P <0.05），而两组的血清Mg2 +相似。这些结果与原发性高血压的血小板中Mg2 +缺乏假说相反。

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