Summary:The changes of Na,K-ATPase activity and its regulation have been investigated in the renal cortex and its basolateral membrane of aldosterone-induced hypertensive rat. Ouabain-sensitive Na,K-ATPase activity and [ 3 H]ouabain-binding site (Bmax) in the hypertensive rat were significantly increased than those in the control. The levels of Na,KATPase α,-and β,-subunit mRNA of the renal cortex in hypertensive rat were more increased than those in the control, and their increases were repressed by actinomycin-D. These results suggest that the increase of Na,K-ATPase activities and ouabain binding sites in aldosterone-induced hypertensive rat may be correlated with transcriptional regulation of Na,K-ATPase gene expression.Key Words: Na,K-ATPase, Ouabain-binding site, Aldosterone, Hypertension Na,K-ATPase (NKA) is a transmembrane pump responsible for the maintenance of sodium and potassium electrochemical gradients across cell membranes. It is composed of a catalytic α,-subunit (a, ot 2> anda 3 ) and a ß-subunit (ß, and ß 2 ) of unknown function (1,2). In the kidney, it is a protein in mediating Na-transport (3), and exists exclusively in the α,/β, form (4,5).NKA activity related to Na + and K + transport in the renal tubule of the rat is regulated by adrenal corticoids (6,7). Aldosterone increases the number of apical membrane Na-channels, but has not an effect on Na-pump itself (8). However, Verrey et al. (9) have shown that aldosterone can induce the Na-pump during the late phase of the hormone's action in cultured kidney cells, and Barlet-Bas et al. (10) also have shown that aldosterone can directly increase NKA activity in vitro in rat cortical collecting tubule. Such a discrepancy remains to be resolved. When aldosterone was infused subcutaneously to evaluate the long-term in vivo effect on NKA activity and change of mRNA of ΝΚΑα,-and β,-subunit in rat kidney, some of them were changed. So we report the results in this paper.
The changes of Na,K‐ATPase activity and its regulation have been investigated in the renal cortex of 1‐clip‐1‐kidney hypertensive rat. Ouabain‐sensitive Na,K‐ATPase activity (Emax) and [3H]ouabain‐binding site (Bmax) in the hypertensive rat were slightly increased than those in the control. The levels of Na,K‐ATPase α1‐ and β1‐subunit mRNA of the renal cortex in hypertensive rat were more increased than those in the control. Their increases were repressed by actinomycin‐D, but not altered or more increased by cycloheximide. These results suggest that the increase of Na,K‐ATPase activities and ouabain binding sites in 1‐clip‐1‐kidney hypertensive rat may be correlated with the increases of gene expression in transcription level and/or of mRNA stability of Na,K‐ATPase.
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