Gless K H, Sütterlin U, Schaz K, Schütz V, Hunstein W
Clin Physiol Biochem. 1986;4(3):199-209.
Intracellular sodium content ([Nai]), ouabain-sensitive ('Na-K ATPase') and ouabain-insensitive ('passive permeability') sodium efflux, Na-K cotransport and Na-Li ('Na-Na') countertransport were estimated in erythrocytes in 39 control subjects, 20 patients with essential hypertension, 14 patients with hypokalemia of renal or unknown etiology, 13 hyperthyroid patients and 19 pregnant women. In normokalemic essential hypertension there was only a moderate, but significant elevation of the activity of the Na-Li countertransport system. In the group of patients with hypokalemia, there was a significant increase of [Nai], ouabain-insensitive sodium efflux and Na-Li countertransport. In hyperthyroidism, a marked decrease of Na-Li countertransport was associated with a marked elevation of [Nai], in pregnancy an elevation of the Na-Li countertransport with a [Nai] 43% lower than the control values. The ouabain-sensitive sodium efflux was elevated in hyperthyroidism and hypokalemia, in which [Nai] was increased. In the control subjects there was a positive linear correlation between ouabain-sensitive sodium efflux and [Nai]. The sodium component of the Na-K cotransport was decreased to about one third of the unchanged furosemide-sensitive potassium component during pregnancy.
The changes of cellular sodium metabolism in essential hypertension are of minor degree as compared to those in the other conditions studied. Cellular sodium metabolism in blood cells is influenced by thyroid hormones and metabolic disorders. Na-Li countertransport, i.e. Na-Na countertransport, seems to be involved in the regulation of [Nai]: an increase of its activity diminishes [Nai] (pregnancy); a decrease elevates [Nai] (hyperthyroidism). Ouabain-sensitive sodium efflux, i.e. 'Na-K ATPase', is mainly regulated by its substrate, [Nai].
在39名对照受试者、20名原发性高血压患者、14名病因不明或肾脏原因导致低钾血症的患者、13名甲状腺功能亢进患者和19名孕妇的红细胞中，估计了细胞内钠含量（[Nai]）、哇巴因敏感的（“钠钾ATP酶”）和哇巴因不敏感的（“被动通透性”）钠外流、钠钾协同转运和钠锂（“钠-钠”）逆向转运。在正常血钾的原发性高血压中，钠锂逆向转运系统的活性仅适度但显著升高。在低钾血症患者组中，[Nai]、哇巴因不敏感的钠外流和钠锂逆向转运显著增加。在甲状腺功能亢进时，钠锂逆向转运显著降低，同时[Nai]显著升高；在妊娠时，钠锂逆向转运升高，而[Nai]比对照值低43%。哇巴因敏感的钠外流在甲状腺功能亢进和低钾血症时升高，此时[Nai]增加。在对照受试者中，哇巴因敏感的钠外流与[Nai]之间存在正线性相关。在妊娠期间，钠钾协同转运的钠成分降至未改变的速尿敏感钾成分的约三分之一。
与所研究的其他情况相比，原发性高血压中细胞钠代谢的变化程度较小。血细胞中的细胞钠代谢受甲状腺激素和代谢紊乱的影响。钠锂逆向转运，即钠-钠逆向转运，似乎参与了[Nai]的调节：其活性增加会降低[Nai]（妊娠）；活性降低会升高[Nai]（甲状腺功能亢进）。哇巴因敏感的钠外流，即“钠钾ATP酶”，主要受其底物[Nai]的调节。
