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Am J Physiol Endocrinol Metab 275: E1072-E1081, 1998;
0193-1849/98 $5.00
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Vol. 275, Issue 6, E1072-E1081, December 1998

Adrenal-dependent modulation of the catalytic subunit isoforms of the Na+-K+-ATPase in aorta

Luis Michea, Viviana Valenzuela, Ignacio Bravo, Andrés Schuster, and Elisa T. Marusic

Laboratory of Molecular and Cellular Physiology, School of Medicine, University Los Andes, Casilla 20106, Santiago 20-Chile

Na+-K+-ATPase gene expression and activity were studied in aortas from adrenalectomized (ADX) rats and ADX rats with deoxycorticosterone supplement (ADX-DOCA). Northern analysis of RNA from ADX rats revealed a significant decrease in alpha 2-mRNA levels (38.5 ± 8.3% of control, P < 0.01) that was prevented by DOCA (P < 0.05). A decrease to 55.8 ± 7.7% in alpha 2-isoform protein was observed 8 days after adrenal removal (P < 0.05); DOCA reversed this effect (90.8 ± 10.5%). Adrenalectomy induced a decrease of 68.5 ± 4.5% in beta 1-mRNA (P < 0.01) and 52.7 ± 8.3% in ADX-DOCA rats (P < 0.01). Also, a reduction in beta 1-isoform protein that was not prevented by DOCA was detected after adrenalectomy (47.1 ± 11%, P < 0.01). In contrast, no differences in alpha 1-mRNA or -protein levels were observed. Vascular sodium pump activity was reduced to 59.8 ± 4.6% of control values after adrenalectomy (P < 0.01); this reduction was reversed by DOCA. Our data indicate that corticosteroids regulate Na+-K+-ATPase isoform expression and activity in vascular tissue in vivo, suggesting a mineralocorticoid-dependent modulation of alpha 2-Na+-K+-ATPase gene expression in aorta, with beta 1-isoform expression dependent on the presence of glucocorticoids.

vascular smooth muscle cells; aldosterone; hypertension


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