Swales J D
Biosci Rep. 1982 Dec;2(12):967-90. doi: 10.1007/BF01122165.
A wide range of abnormalities of membrane sodium and potassium transport can be demonstrated in patients with essential hypertension, and in rats with genetic hypertension and with some forms of experimental hypertension. In the human red cell increased permeability to sodium and potassium, increased ouabain-sensitive sodium pumping, lithium-sodium counter-transport, and frusemide-sensitive co-transport have been described; by contrast, in the human leucocyte sodium pumping is reduced. In the spontaneously hypertensive rat and the rat with mineralocorticoid-induced hypertension, increased permeability to sodium and potassium, with increased ouabain-sensitive pumping, is shared by the red cell and the arterial smooth muscle. This abnormality is associated with decreased cell-membrane affinity for calcium and increased cell-membrane viscosity. It is proposed that in essential hypertension the decreased membrane affinity for calcium is a primary pathogenetic change giving rise to secondary changes in sodium and potassium transport.
在原发性高血压患者、遗传性高血压大鼠以及某些形式的实验性高血压大鼠中，均可证实存在多种膜钠和钾转运异常。在人类红细胞中，已发现对钠和钾的通透性增加、哇巴因敏感的钠泵活性增强、锂-钠逆向转运以及速尿敏感的协同转运；相比之下，人类白细胞中的钠泵活性降低。在自发性高血压大鼠和盐皮质激素诱导性高血压大鼠中，红细胞和动脉平滑肌对钠和钾的通透性增加，同时哇巴因敏感的泵活性增强。这种异常与细胞膜对钙的亲和力降低以及细胞膜粘度增加有关。有人提出，在原发性高血压中，细胞膜对钙的亲和力降低是一种原发性致病变化，可导致钠和钾转运的继发性变化。
