Fujita T, Noda H, Ando K, Sato Y
Life Sci. 1983 Apr 4;32(14):1621-7. doi: 10.1016/0024-3205(83)90869-x.
We have studied ouabain-resistant, external sodium-stimulated, lithium efflux (Li-Na countertransport) in red blood cells from 21 borderline hypertensives with at least one hypertensive first degree relative (BH-F), 19 borderline hypertensives without family history of essential hypertension (BH-NF), and 35 age-matched normotensive subjects. The data indicate the finding of an increased Li-Na countertransport in all BH (F+NF), but with a significant overlap between BH values and control ones: Li-Na countertransport is significantly higher only in BH-F but it is normal in BH-NF. Moreover, there is a significant correlation of Li-Na countertransport to total peripheral resistance but not to mean blood pressure in all hypertensive patients. It is suggested that in BH the increase of erythrocyte Na flux is mediated by the Na-Na exchange diffusion, and its abnormality may be associated to the hereditary trait of essential hypertension rather than the high blood pressure per se, probably resulting in the development of hypertension, through the increased vascular smooth muscle tone.
我们研究了21名至少有一位高血压一级亲属的临界高血压患者（BH-F）、19名无原发性高血压家族史的临界高血压患者（BH-NF）以及35名年龄匹配的血压正常受试者红细胞中的哇巴因抵抗性、外源性钠刺激的锂外流（锂-钠逆向转运）。数据表明，所有临界高血压患者（F+NF）均存在锂-钠逆向转运增加的情况，但临界高血压患者的值与对照组的值有显著重叠：仅BH-F组的锂-钠逆向转运显著更高，而BH-NF组则正常。此外，在所有高血压患者中，锂-钠逆向转运与总外周阻力显著相关，但与平均血压无关。提示在临界高血压患者中，红细胞钠通量的增加是由钠-钠交换扩散介导的，其异常可能与原发性高血压的遗传特征有关，而非高血压本身，可能通过增加血管平滑肌张力导致高血压的发生。
