1例青少年原发性高血压:红细胞净Na+、K+通量测定的意义。

J L Elghozi, G Dagher, R P Garay, D Vasmant, F Girard, P Meyer
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引用次数: 0

摘要

近年来研究报道了一种遗传性膜缺陷,它与原发性高血压的发生密切相关。这种异常是由原发性高血压患者和高血压父母所生的一些血压正常者红细胞中Na+—K+共运输机制的功能缺陷组成的。这里我们报告一例青少年原发性高血压,包括家族性红细胞Na+, K+的测量。2岁男童患有原发性高血压,并有异常,Na+, K+泵无代偿活性。这位母亲在怀孕期间患上了高血压。由于净Na+/K+通量比降低,她的红细胞也出现异常。一个姐妹也有同样的异常,但没有高血压,但对该患者的Na+挤压机制的完整分析表明Na+, K+泵活性的代偿作用。其他家庭成员血压正常,无血流异常。因此,红细胞通量测量可能对青少年高血压的诊断和遗传有意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A case of juvenile essential hypertension: implications of erythrocyte net Na+, K+ flux measurement.

In recent studies were reported an inherited membrane defect which is closely related to the development of essential hypertension. This abnormality consists of a functional deficiency in the Na+--K+ co-transport mechanism in erythrocytes of essential hypertensives and some normotensives born of hypertensive parents. Here we report a case of juvenile essential hypertension including familial erythrocyte Na+, K+ measurements. The 2-year-old boy had essential hypertension and bore the abnormality, with no compensatory activity of the Na+, K+ pump. The mother had developed hypertension during pregnancy. She also bore the erythrocyte abnormality as the net Na+/K+ flux ratio was reduced. One sister bore the same abnormality without hypertension but a complete analysis of Na+ extrusion mechanisms in this patient demonstrated a compensatory effect of the Na+, K+ pump activity. Other members of the family were normotensive without the flux abnormality. It appears therefore that erythrocyte flux measurements might be of diagnostic and genetic interest in juvenile hypertension.

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