TORIYABE, S., MIURA, Y., KIMURA, S., MEGURO, Y., SUGAWARA, T., NOSHIRO, T., TAKAHASHI, M., OHASHI, H., SANO, N., WATANABE, H. and YOSHINAGA, K.
A Plasma Inhibitor of Sodium and Potassium Activated Adenosine Triphosphatase in Patients with Essential Hypertension. Tohoku J. exp. Med., 1988,
155 (2), 129-137 - 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<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 30sec, 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 500μg/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. This study may also raise a question whether plasma free NKI, supposedly an active from of NKI, is actually working as a physiological regulator in vivo. It seems thus premature to assume it as a pathogenic factor in essential hypertension.
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