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单肾单夹高血压大鼠心肌钠钾ATP酶活性降低。

Decreased myocardial Na+-K+-ATPase activity in one-kidney, one-clip hypertensive rats.

作者信息

Clough D L, Pamnani M B, Haddy F J

出版信息

Am J Physiol. 1983 Aug;245(2):H244-51. doi: 10.1152/ajpheart.1983.245.2.H244.

Abstract

We have previously shown that Na+-K+ pump activity (ouabain-sensitive 86Rb uptake) is decreased in vascular tissue of animals with various forms of low renin hypertension. In the present study we measured Na+-K+-ATPase activity, the energy source for Na+-K+ pumping, in membrane fractions prepared from myocardial tissue of rats with chronic one-kidney, one-clip hypertension and their one-kidney normotensive controls. Membranes were prepared by two independent methods: microsomal fractions (method 1) and fractions prepared by the hypotonic LiBr method of Dhalla et al. (method 2). In membranes prepared from left ventricles of the hypertensive rats (by method 1) Na+-K+-ATPase activity was decreased, Mg2+-ATPase activity was increased, and the sialic acid content and 5'-nucleotidase activity (two putative membrane markers) were unchanged relative to the control rats. The sensitivity of cardiac Na+-K+-ATPase to inhibition by ouabain was also unchanged. Na+-K+-ATPase activity was also decreased in the right ventricles (method 1) of these hypertensive rats, suggesting that this defect is probably not pressure related. In membranes prepared from the left ventricles of the hypertensive rats by method 2, Na+-K+-ATPase activity was again reduced, whereas the Mg2+-ATPase and 5'-nucleotidase activities were unchanged relative to the controls. These studies suggest that myocardial Na+-K+-ATPase activity is suppressed in rats with this low renin form of hypertension and the possible effect of this suppression on myocardial contractile activity is discussed.

摘要

我们之前已经表明,在患有各种形式低肾素性高血压的动物的血管组织中,钠钾泵活性(哇巴因敏感的⁸⁶Rb摄取)降低。在本研究中,我们测量了慢性单肾单夹高血压大鼠及其单肾血压正常对照大鼠心肌组织制备的膜组分中钠钾ATP酶活性,这是钠钾泵的能量来源。通过两种独立方法制备膜:微粒体组分(方法1)和通过Dhalla等人的低渗溴化锂方法制备的组分(方法2)。在由高血压大鼠左心室制备的膜(通过方法1)中,相对于对照大鼠,钠钾ATP酶活性降低,镁ATP酶活性增加,唾液酸含量和5'-核苷酸酶活性(两种假定的膜标志物)未改变。心脏钠钾ATP酶对哇巴因抑制的敏感性也未改变。这些高血压大鼠右心室(方法1)中的钠钾ATP酶活性也降低,表明这种缺陷可能与压力无关。在通过方法2由高血压大鼠左心室制备的膜中,钠钾ATP酶活性再次降低,而相对于对照,镁ATP酶和5'-核苷酸酶活性未改变。这些研究表明,在患有这种低肾素形式高血压的大鼠中,心肌钠钾ATP酶活性受到抑制,并讨论了这种抑制对心肌收缩活动的可能影响。

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