原发性高血压患者红细胞中钠钾协同转运系统的遗传性缺陷。

Inherited defect in a Na+, K-co-transport system in erythrocytes from essential hypertensive patients.

作者信息

Garay R P, Dagher G, Pernollet M G, Devynck M A, Meyer P

出版信息

Nature. 1980 Mar 20;284(5753):281-3. doi: 10.1038/284281a0.

Abstract

The Na+ and K+ electrochemical gradients across cell membranes are believed to be maintained by the action of a Na+, K+-pump. In human erythrocytes this pump exchanges internal Na+ for external K+ in approximately a 1.5 ratio. Thus, when Na+-loaded/K+-depleted erythrocytes are incubated in physiological conditions they tend to recover their original low Na+/high K+ content. Surprisingly, in erythrocytes from healthy donors the net Na+ extrusion/K+ influx ratio exceeds the 1.5 ratio predicted for Na+, K+-pump-mediated fluxes whereas it is similar to this value in erythrocytes from essential hypertensive patients and some of their descendants. We now report that this difference is due to the presence of a Na+, K+-co-transport system in normal erythrocytes which extrudes both internal Na+ and K+ and is functionally deficient in erythrocytes of essential hypertensive patients and some of their descendants. No difference in passive Na+ permeability could be detected between normotoensive and hypertensive subjects.

摘要

细胞膜两侧的Na⁺和K⁺电化学梯度被认为是由Na⁺,K⁺-泵的作用来维持的。在人类红细胞中，这种泵以大约1.5的比例将细胞内的Na⁺与细胞外的K⁺进行交换。因此，当装载Na⁺/耗尽K⁺的红细胞在生理条件下孵育时，它们倾向于恢复其原来的低Na⁺/高K⁺含量。令人惊讶的是，在健康供体的红细胞中，净Na⁺外排/K⁺内流比例超过了Na⁺,K⁺-泵介导通量所预测的1.5比例，而在原发性高血压患者及其一些后代的红细胞中，该比例与此值相似。我们现在报告，这种差异是由于正常红细胞中存在一种Na⁺,K⁺-共转运系统，该系统可排出细胞内的Na⁺和K⁺，而在原发性高血压患者及其一些后代的红细胞中，该系统功能存在缺陷。在血压正常和高血压受试者之间未检测到被动Na⁺通透性的差异。