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原发性高血压患者体内钠钾激活的三磷酸腺苷酶的血浆抑制剂

A plasma inhibitor of sodium and potassium activated adenosine triphosphatase in patients with essential hypertension.

作者信息

Toriyabe S, Miura Y, Kimura S, Meguro Y, Sugawara T, Noshiro T, Takahashi M, Ohashi H, Sano N, Watanabe H

机构信息

Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai.

出版信息

Tohoku J Exp Med. 1988 Jun;155(2):129-37. doi: 10.1620/tjem.155.129.

DOI:10.1620/tjem.155.129
PMID:2850642
Abstract

The purpose of this study is to evaluate the plasma Na, K-ATPase inhibitor (NKI) in patients with essential hypertension and to compare the mode of its biochemical actions on the Na, K-ATPase with that of ouabain. Plasma NKI was extracted through a reversed-phase cartridge column and its inhibitory action on hog brain Na, K-ATPase was measured in vitro. Plasma NKI activity was significantly greater in patients with essential hypertension (44 +/- 2.8% (S.E.), n = 28, p less than 0.01) than in normotensive controls (25 +/- 2.4%, n = 21). No significant correlation was demonstrated between the values of plasma NKI and mean arterial pressure in either group. Both plasma NKI and ouabain showed a dose-dependent inhibition on the Na, K-ATPase reaction. An action of ouabain was competitively antagonized by increased concentration of potassium in the reaction mixture, while plasma NKI showed a constant inhibition on the Na, K-ATPase independently of potassium concentrations. The action of plasma NKI was of rapid onset and linear with time, while ouabain showed a delayed onset of the reaction over 30 sec, followed by a progressively increasing inhibition on the enzyme reaction. Finally, the inhibitory action of plasma NKI on Na, K-ATPase was completely abolished in the presence of bovine serum albumin even at the concentration of 500 micrograms/ml in the reaction mixture, which did not have any influence on the actions of ouabain. To sum up, the results showed a markedly different nature of plasma NKI from ouabain in the mode of biochemical actions on the Na, K-ATPase in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究旨在评估原发性高血压患者血浆钠钾 -ATP酶抑制剂(NKI),并比较其对钠钾 -ATP酶的生化作用模式与哇巴因的异同。通过反相柱提取血浆NKI,并在体外测定其对猪脑钠钾 -ATP酶的抑制作用。原发性高血压患者的血浆NKI活性(44±2.8%(标准误),n = 28,p<0.01)显著高于血压正常对照组(25±2.4%,n = 21)。两组中血浆NKI值与平均动脉压之间均未显示出显著相关性。血浆NKI和哇巴因对钠钾 -ATP酶反应均表现出剂量依赖性抑制。反应混合物中钾浓度升高可竞争性拮抗哇巴因的作用,而血浆NKI对钠钾 -ATP酶的抑制作用与钾浓度无关。血浆NKI的作用起效迅速且呈时间线性关系,而哇巴因在30秒后反应延迟开始,随后对酶反应的抑制作用逐渐增强。最后,即使反应混合物中牛血清白蛋白浓度为500微克/毫升,血浆NKI对钠钾 -ATP酶的抑制作用也完全被消除,而这对哇巴因的作用没有任何影响。总之,结果表明,在体外对钠钾 -ATP酶的生化作用模式方面,血浆NKI与哇巴因具有明显不同的性质。(摘要截短至250字)

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