Losse H, Zidek W, Zumkley H, Wessels F, Vetter H
Clin Exp Hypertens (1978). 1981;3(4):627-40. doi: 10.3109/10641968109033689.
In 1960 the pathophysiological mechanisms by which Na+ is involved in human essential hypertension were first elucidated by the finding that intracellular Na+ is elevated in red blood cells of essential hypertensives. Furthermore it was found that (1) transmembranous Na+ fluxes in red blood cells of essential hypertensives are changed in parallel with intracellular Na+ concentration, reflecting the metabolic disturbances better than the Na+ concentration measurements, (2) in normotensives with a familial disposition of essential hypertension intracellular Na+ and transmembranous Na+ fluxes are elevated, (3) uremia affects intracellular Na+ levels similarly as essential hypertension, and (4) intracellular free Na+ and free Ca++ is increased in spontaneously hypertensive rats. It can be assumed that elevated intracellular Na+ plays a causative role in essential hypertension.
1960年，通过发现原发性高血压患者红细胞内的钠离子浓度升高，钠离子参与人类原发性高血压的病理生理机制首次得到阐明。此外，还发现：（1）原发性高血压患者红细胞的跨膜钠离子通量与细胞内钠离子浓度平行变化，与钠离子浓度测量相比，能更好地反映代谢紊乱；（2）有原发性高血压家族倾向的血压正常者，其细胞内钠离子和跨膜钠离子通量升高；（3）尿毒症对细胞内钠离子水平的影响与原发性高血压相似；（4）自发性高血压大鼠的细胞内游离钠离子和游离钙离子增加。可以推测，细胞内钠离子升高在原发性高血压中起致病作用。
