人和大鼠红细胞中阳离子转运和多磷酸肌醇代谢的体积依赖性调节:原发性高血压的特征。

Physiologia Bohemoslovaca Pub Date : 1990-01-01
S N Orlov, N I Pokudin, P V Gulak, Postnov YuV
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摘要

在原发性高血压(EH)患者和自发性高血压大鼠(SHR)中,δ mu H+诱导的红细胞Na+/H+交换率升高。仅SHR红细胞中Na+、K(+)-共转运增加。在年轻红细胞和老年红细胞中均观察到这种改变以及平均细胞体积的减少。大鼠(而不是人)红细胞的适度收缩导致Na+,K(+)-共转运率的增加。大鼠(而不是人)红细胞更明显的收缩诱导Na+/H+交换。这些反应伴有磷酸肌苷反应。蛋白激酶C激活剂(TPA)在人和大鼠红细胞中增加δ mu H+诱导的Na+/H+交换,但不改变磷酸肌苷代谢。经tpa处理的SHR红细胞与WKY红细胞Na+/H+交换率无差异。我们假设蛋白激酶C的激活增加了原发性高血压患者的Na+/H+交换。原发性高血压实验模型显示Na+/H(+)-共转运增加可能是由于红细胞体积减少所致。
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Volume-dependent regulation of cation transport and polyphosphoinositide metabolism in human and rat erythrocytes: features revealed in primary hypertension.

The rate of delta mu H+ --induced erythrocyte Na+/H+ exchange is increased in both patients with essential hypertension (EH) and spontaneously hypertensive rats (SHR). The increase of Na+,K(+)-cotransport was revealed in erythrocytes of SHR only. This alteration as well as a decrease of mean cell volume were observed in both young and old erythrocytes of SHR. The moderate shrinkage of rat (but not human) erythrocytes results in an increase of the rate of Na+,K(+)-cotransport. The more pronounced shrinkage of rat (but not human) erythrocytes induces the Na+/H+ exchange. These reactions are accompanied by phosphoinositide response. Activator of protein kinase C (TPA) increases delta mu H+ --induced Na+/H+ exchange both in human and rat erythrocytes but it does not modify phosphoinositide metabolism. No differences were observed in the rate of Na+/H+ exchange between TPA-treated erythrocytes of SHR and WKY. We assume that the activation of protein kinase C increases Na+/H+ exchange in primary hypertension. Increased Na+/H(+)-cotransport revealed in an experimental model of primary hypertension is probably due to the decrease of erythrocyte volume.

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