正常血压和自发性高血压大鼠体内急性钠负荷后的细胞膜变化。

Cell membrane changes after in vivo acute Na+ load in normotensive and spontaneously hypertensive rats.

作者信息

De Mendonca M, Grichois M L, Dagher G, Aragon-Birloues I, Montenay-Garestier T, Devynck M A, Meyer P

出版信息

Clin Exp Hypertens A. 1984;6(9):1559-74. doi: 10.3109/10641968409044069.

DOI:10.3109/10641968409044069

Abstract

Our previous observation of a greater increase in erythrocyte Na+ in SHR than in WKY after an acute Na+ load may result either from a genetic membrane property or from a specific plasma influence. In order to elucidate this question, membrane characteristics were compared with or without an acute Na+ load. Na+ transport was measured in Ringer and in plasma on Na+ enriched and K+ depleted red cells. Platelet microviscosity was measured as an index of membrane structural changes. After acute Na+ load a similar reduction of net Na+ extrusion and of K+ influx was observed in both strains. This indicates an inhibition of the Na+,K+-pump. Platelet microviscosity was similarly increased in SHR and WKY. Thus an acute Na+ load induced alterations of membrane properties in both SHR and WKY. The higher erythrocyte Na+ content in SHR stems rather from their intrinsic membrane properties than from a plasma factor.

摘要

我们之前观察到，急性钠负荷后，自发性高血压大鼠（SHR）红细胞钠的增加幅度大于正常血压大鼠（WKY），这可能是由于遗传膜特性或特定血浆影响所致。为了阐明这个问题，我们比较了有或没有急性钠负荷时的膜特性。在富含钠和低钾的红细胞的林格液和血浆中测量钠转运。测量血小板微粘度作为膜结构变化的指标。急性钠负荷后，在两个品系中均观察到净钠排出和钾流入的类似减少。这表明钠钾泵受到抑制。SHR和WKY的血小板微粘度同样增加。因此，急性钠负荷在SHR和WKY中均诱导了膜特性的改变。SHR中较高的红细胞钠含量更多地源于其内在膜特性，而非血浆因子。