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肾单位减少-盐性高血压大鼠心肌钠钾ATP酶活性降低

Decreased myocardial Na+K+ATPase activity in rats with reduced renal mass-saline hypertension.

作者信息

Clough D L, Huot S J, Pamnani M B, Haddy F J

出版信息

J Hypertens. 1985 Dec;3(6):583-9. doi: 10.1097/00004872-198512000-00003.

Abstract

Inhibition of cardiovascular Na,K-pump activity has been shown to promote an increase in the contractile activity of myocardial and vascular smooth muscle and a consequent rise in blood pressure (BP). It has also been shown that vascular Na,K-pump activity and myocardial Na+K+ATPase activity [the energy source for active sodium (Na) and potassium (K) transport] are decreased in rats with various forms of low renin hypertension including rats with reduced renal mass-saline (RRM-saline) hypertension. In the present study, left ventricular Na+K+ATPase activity from rats with RRM-saline hypertension was found to be decreased in membranes prepared by two independent methods: deoxycholate, sodium iodide (Nal)-treated microsomal fractions (method 1) and membranes prepared by the hypotonic, lithium bromide (LiBr) method (method 2). Relative to RRM normotensive control rats which drank distilled water, myocardial Na+K+ATPase activity from RRM-saline drinking rats was decreased by 18.2% in membranes prepared by method 1 and 33.6% in membranes prepared by method 2. The apparent affinities of Na+K+ATPase for K and for ouabain were unaltered relative to controls in membranes prepared from these hypertensive rats by method 1, and the sialic acid content and 5'-nucleotidase activity (two putative sarcolemmal markers) were unaltered in membranes from the hypertensive rats, prepared by methods 1 and 2 respectively. The Mg2+ATPase activity of membranes prepared by method 1 was increased in the RRM-saline hypertensive rats but because it was not increased in membranes prepared by method 2 the former observation does not appear to be of any pathophysiological importance. In other experiments, hypertension was reversed in RRM-saline hypertensive rats by restricting their salt intake (substitution of distilled water for drinking).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

已有研究表明,抑制心血管系统的钠钾泵活性会促使心肌和血管平滑肌的收缩活性增强,进而导致血压升高。研究还显示,在各种低肾素性高血压大鼠中,包括肾质量减少-生理盐水(RRM-生理盐水)高血压大鼠,血管钠钾泵活性和心肌钠钾ATP酶活性(主动钠和钾转运的能量来源)会降低。在本研究中,通过两种独立方法制备的膜中,发现RRM-生理盐水高血压大鼠的左心室钠钾ATP酶活性降低:脱氧胆酸盐、碘化钠(Nal)处理的微粒体组分(方法1)以及通过低渗溴化锂(LiBr)方法制备的膜(方法2)。相对于饮用蒸馏水的RRM正常血压对照大鼠,饮用生理盐水的RRM-生理盐水大鼠的心肌钠钾ATP酶活性在方法1制备的膜中降低了18.2%,在方法2制备的膜中降低了33.6%。通过方法1从这些高血压大鼠制备的膜中,钠钾ATP酶对钾和哇巴因的表观亲和力相对于对照未发生改变,并且分别通过方法1和2制备的高血压大鼠膜中的唾液酸含量和5'-核苷酸酶活性(两种假定的肌膜标志物)也未改变。方法1制备的膜的Mg2+ATP酶活性在RRM-生理盐水高血压大鼠中升高,但由于方法2制备的膜中未升高,所以前一观察结果似乎没有任何病理生理学意义。在其他实验中,通过限制RRM-生理盐水高血压大鼠的盐摄入量(用蒸馏水替代饮用水)可使高血压得到逆转。(摘要截短于250字)

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