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正常血压大鼠和自发性高血压大鼠肾脏中的利钠作用及肾钠钾ATP酶活性

Natriuresis and renal Na-K-ATPase activity in kidneys of normotensive and spontaneously hypertensive rats.

作者信息

Slegers J F, Förster M T

出版信息

Miner Electrolyte Metab. 1982 Jul;8(1):21-8.

PMID:6132327
Abstract

The isolated perfused kidneys of spontaneously hypertensive (SHR) rats aged 10-12 weeks (early hypertensive phase) exhibited pressure natriuresis curves already shifted to the right, as compared with kidneys of the normotensive Wistar rats and Wistar-Kyoto rats. Sodium excretion in relation to tubular sodium load was higher in kidneys of SHR rats as compared with those of the normotensive controls. Renal Na-K-ATPase activity was significantly lowered only in the cortex during chronic hypertension but not in the outer medulla. In both parts of the kidney no differences could be detected in the apparent Km value for sodium stimulation or the apparent activation energies. Mg-ATPase activity was lowered in SHR rats during chronic hypertension. Protein content was significantly decreased in the outer medulla of SHR rats in the early hypertensive phase as well as during chronic hypertension. The results suggest that the functional changes observed in kidneys of young SHR rats are not due to a genetically determined defect in renal Na-K-ATPase.

摘要

与正常血压的Wistar大鼠和Wistar-Kyoto大鼠的肾脏相比,10-12周龄(高血压早期)自发性高血压(SHR)大鼠的离体灌注肾脏表现出压力利尿曲线已向右移位。与正常血压对照组相比,SHR大鼠肾脏中与肾小管钠负荷相关的钠排泄更高。仅在慢性高血压期间,肾Na-K-ATP酶活性在皮质中显著降低,但在外髓质中未降低。在肾脏的两个部分中,钠刺激的表观Km值或表观活化能均未检测到差异。慢性高血压期间,SHR大鼠的Mg-ATP酶活性降低。在高血压早期以及慢性高血压期间,SHR大鼠外髓质中的蛋白质含量显著降低。结果表明,在年轻SHR大鼠肾脏中观察到的功能变化并非由于肾Na-K-ATP酶的遗传缺陷所致。

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