Heagerty A M, Milner M, Bing R F, Thurston H, Swales J D
Lancet. 1982 Oct 23;2(8304):894-6. doi: 10.1016/s0140-6736(82)90865-0.
Sodium efflux rates were measured in leucocytes from eighteen normotensive subjects who had one or more first-degree relatives with essential hypertension and from twenty-four matched controls with no such family history. The total efflux rate constant was significantly lower in those with a family history of hypertension, owing to reduced ouabain-sensitive sodium pump activity. The presence of a membrane electrolyte handling abnormality characteristic of essential hypertension in normotensive individuals genetically predisposed to hypertension points to an underlying genetic factor. At the same time, the fact that blood-pressure was normal in these subjects indicates that the abnormality does not participate directly in blood-pressure elevation. Rather, the abnormality, like other red-cell changes in electrolyte handling, seems to be a marker for a genetically determined alteration in membrane structure, and thus only indirectly related to hypertension.
在18名有一名或多名原发性高血压一级亲属的血压正常受试者以及24名无此类家族病史的匹配对照者的白细胞中测量了钠流出率。由于哇巴因敏感性钠泵活性降低,有高血压家族史者的总流出率常数显著较低。在遗传上易患高血压的血压正常个体中存在原发性高血压特有的膜电解质处理异常,这表明存在潜在的遗传因素。同时,这些受试者血压正常这一事实表明,该异常并不直接参与血压升高。相反,与电解质处理方面的其他红细胞变化一样,该异常似乎是膜结构遗传决定改变的一个标志,因此仅与高血压间接相关。