van de Ven C J, Bohr D F
Pflugers Arch. 1983 Sep;399(1):74-8. doi: 10.1007/BF00652525.
The goal of this study was to determine whether the elevated flux of sodium and potassium through the erythrocyte membrane of spontaneously hypertensive rats (SHR) is due to an intrinsic difference in the cell membrane or to a humoral factor present in the plasma. Isolated and washed erythrocytes from SHR and normotensive Wistar Kyoto (WKy) and Sprague-Dawley (SD) rats, were incubated in 1) a physiological salt solution, 2) WKy or SD plasma and 3) SHR plasma. Incubations were performed at 4 degrees C for 23 h. Erythrocytes from SHR incubated in physiological salt solution had significantly greater Na+ and K+ fluxes than those from normotensive WKy and SD rats (P less than 0.005). Plasma from any of the three strains of rats, as compared to physiological salt solution, increased Na+ influx in the following order: SD greater than WKy greater than SHR. Erythrocyte K+ efflux was not altered by plasma. We conclude that the elevated flux of Na+ and K+ in SHR erythrocytes is due to an intrinsic difference in the cell membrane. The greater Na+ influx in plasma from any strain of rats is not correlated with the blood pressure of the rat. The lesser increase in Na+ influx in erythrocytes incubated in plasma from SHR masks the greater intrinsic membrane permeability in the SHR erythrocyte when Na+ fluxes are studied in whole blood. The elevated flux of Na+ and K+ through the erythrocyte membrane of SHR may reflect a general membrane defect that underlies the pathogenesis of elevated arterial pressure.
本研究的目的是确定自发性高血压大鼠(SHR)红细胞膜上钠和钾通量的升高是由于细胞膜的内在差异还是血浆中存在的体液因子所致。将SHR以及血压正常的Wistar Kyoto(WKy)和Sprague-Dawley(SD)大鼠的红细胞分离并洗涤后,分别置于1)生理盐溶液、2)WKy或SD血浆以及3)SHR血浆中孵育。孵育在4℃下进行23小时。在生理盐溶液中孵育的SHR红细胞的Na⁺和K⁺通量显著高于血压正常的WKy和SD大鼠的红细胞(P<0.005)。与生理盐溶液相比,三种品系大鼠中任何一种的血浆都会使Na⁺内流按以下顺序增加:SD>WKy>SHR。血浆对红细胞K⁺外流没有影响。我们得出结论,SHR红细胞中Na⁺和K⁺通量的升高是由于细胞膜的内在差异。任何品系大鼠血浆中较高的Na⁺内流与大鼠的血压无关。当在全血中研究Na⁺通量时,在SHR血浆中孵育的红细胞中Na⁺内流增加较少,掩盖了SHR红细胞中较大的内在膜通透性。SHR红细胞膜上Na⁺和K⁺通量的升高可能反映了一种普遍的膜缺陷,这是动脉血压升高发病机制的基础。