Is a circulating sodium transport inhibitor involved in the pathogenesis of essential hypertension?
Is a circulating sodium transport inhibitor involved in the pathogenesis of essential hypertension?
复制标题
循环钠转运抑制剂是否参与原发性高血压的发病机制？
DOI：
10.3109/10641968109033705
复制
发表时间：
1981
影响因子：
12.3
通讯作者：
H. D. de Wardener
中科院分区：
文献类型：
--
作者：
G. MacGregor;H. D. de Wardener
关于钠摄入量与高血压患病率之间的关系存在争议。这一争议部分与钠摄入量增加如何导致外周阻力增加有关。我们提出了以下假设。在原发性高血压患者中，肾脏排钠能力存在遗传性缺陷，随着钠摄入量的增加，这种缺陷变得越来越明显。肾脏钠排泄的困难增加了循环钠转运抑制物的浓度，从而影响了钠在许多细胞膜上的转运。在肾脏中，该抑制剂将尿钠排泄调整回正常水平，从而使钠平衡接近于相同钠摄入量的正常受试者。在小动脉平滑肌中，钠跨细胞壁运输的抑制导致细胞内钠浓度的升高，进而提高细胞内钙浓度，从而增加血管的反应性。这一假说还提出，体内循环细胞钠转运的异常直接是由于循环钠转运抑制物分泌增加所致。讨论了支持这一假说的证据。首先指出，有大量证据表明存在一种循环的Na+-K+-ATPase抑制物，其水平与钠摄入量有关，并且在许多高血压患者中该抑制物的水平似乎升高。其次，高血压患者血浆中孵育的正常血压的白细胞与高血压患者自身的白细胞一样，表现出依赖Na+-K+-ATPase的钠转运的减少，这也表明高血压患者循环中的Na+-K+-ATPase抑制物增加。
There is controversy about the relationship between sodium intake and the prevalence of high blood pressure. Part of this controversy relates to how an increase in sodium intake could cause an increase in peripheral resistance. We have put forward the following hypothesis. In essential hypertension there is an inherited defect of the kidney's ability to excrete sodium which becomes increasingly obvious the greater the sodium intake. This difficulty in sodium excretion by the kidney increases the concentration of a circulating sodium transport inhibitor that affects sodium transport across many cell membranes. In the kidney the inhibitor adjusts urinary sodium excretion back towards normal so that sodium balance is near that of normal subjects on the same intake of sodium. In the arteriolar smooth muscle the inhibition of sodium transport across the cell wall causes a rise in intracellular sodium concentration which, in turn, raises the intracellular calcium concentration and thus increases vascular reactivity. This hypothesis also proposes that the abnormalities of sodium transport in circulating cells in vivo are directly due to the increased secretion of the circulating sodium transport inhibitor. Evidence supporting this hypothesis is discussed. Firstly, it is pointed out that there is much evidence which suggests that there is a circulating inhibitor of Na+-K+-ATPase, the level of which is related to sodium intake and that the level of this inhibitor appears to be increased in many hypertensives. Secondly, the finding that normotensive white cells incubated in the plasma of hypertensive patients develop the same decrease in the Na+-K+-ATPase dependent sodium transport as the hypertensives own white cells also suggests that hypertensives have an increase in a circulating Na+-K+-ATPase inhibitor.