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慢性尿毒症中动脉高血压的发病机制:钠钾ATP酶活性降低的作用。

Pathogenesis of arterial hypertension in chronic uraemia: the role of reduced Na,K-ATPase activity.

作者信息

Boero R, Guarena C, Berto I M, Forneris G, Borca M, Martina G, Quarello F, Piccoli G

机构信息

Institute of Nephro-Urology, University of Torino, Ospedale Nuova Astanteria Martini, Italy.

出版信息

J Hypertens Suppl. 1988 Dec;6(4):S363-5. doi: 10.1097/00004872-198812040-00113.

DOI:10.1097/00004872-198812040-00113
PMID:2853747
Abstract

In 38 uraemic dialysed patients (17 normotensive, 21 hypertensive) we measured (1) erythrocyte sodium concentration [Nai] and ouabain-sensitive sodium efflux, and (2) arterial pressure, cardiac index and total peripheral resistance. Erythrocyte Na-K pump activity was lower in hypertensive than in normotensive patients (P less than 0.02). Hypertensive patients had significantly higher peripheral resistance than normotensive patients (P less than 0.05), while the cardiac index was similar in both groups. Inverse correlations were found between the rate constant for ouabain-sensitive sodium efflux in erythrocytes and both systolic and diastolic pressure (r = -0.43 and r = -0.45, respectively; P less than 0.01) and total peripheral resistance (r = -0.76; P less than 0.0001). Our data suggest that reduced sodium transport by the Na-K pump plays a role in the pathogenesis of arterial hypertension in patients with chronic uraemia.

摘要

在38例接受透析的尿毒症患者(17例血压正常,21例高血压)中,我们测量了:(1)红细胞钠浓度[Nai]和哇巴因敏感的钠外流;(2)动脉压、心脏指数和总外周阻力。高血压患者的红细胞钠钾泵活性低于血压正常患者(P<0.02)。高血压患者的外周阻力显著高于血压正常患者(P<0.05),而两组的心脏指数相似。红细胞中哇巴因敏感的钠外流速率常数与收缩压和舒张压(分别为r=-0.43和r=-0.45;P<0.01)以及总外周阻力(r=-0.76;P<0.0001)之间存在负相关。我们的数据表明,钠钾泵介导的钠转运减少在慢性尿毒症患者动脉高血压的发病机制中起作用。

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Pathogenesis of arterial hypertension in chronic uraemia: the role of reduced Na,K-ATPase activity.慢性尿毒症中动脉高血压的发病机制:钠钾ATP酶活性降低的作用。
J Hypertens Suppl. 1988 Dec;6(4):S363-5. doi: 10.1097/00004872-198812040-00113.
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