Regulation of Na-K-ATPase gene expression by aldosterone in vascular smooth muscle cells.
Am J Physiol
; 265(4 Pt 2): H1167-72, 1993 Oct.
Article
em En
| MEDLINE
| ID: mdl-8238401
ABSTRACT
Na-K-adenosinetriphosphatase (ATPase) activity profoundly influences vascular cell excitability, contractility, and volume regulation. The recent finding of mineralocorticoid hormone receptors in vascular tissue suggests the possibility that Na-K-ATPase gene expression in vascular tissue is regulated by the mineralocorticoid aldosterone. In this study, we investigated Na-K-ATPase gene expression by aldosterone in cultured rat vascular smooth muscle cells (VSMC). Na-K-ATPase alpha 1- and beta 1-isoform mRNAs, but not alpha 2- and alpha 3-isoform mRNAs, were expressed in cultured rat VSMC. Aldosterone caused a 2.3-fold increase in the alpha 1 mRNA and a 4.7-fold increase in the beta 1 mRNA accumulation with peak elevations at 24 and 6 h, respectively. Aldosterone induced the alpha 1 mRNA expression at physiological concentrations (half-maximum effective concentration = 2-3 nM), consistent with the binding of aldosterone to mineralocorticoid hormone receptors. The augmented alpha 1 mRNA expression by aldosterone was associated with a twofold increase in the alpha 1-subunit protein accumulation. Pretreatment of VSMC with cycloheximide caused a 10-fold increase in the alpha 1 mRNA expression, and the aldosterone-mediated alpha 1 mRNA accumulation was not observed in the presence of cycloheximide. Transfection experiments with the luciferase reporter gene revealed that aldosterone response sequences are located within the 5'-flanking regions of the alpha 1-isoform gene. These data demonstrate that the mineralocorticoid aldosterone directly stimulates Na-K-ATPase gene expression and protein accumulation in VSMC.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Expressão Gênica
/
ATPase Trocadora de Sódio-Potássio
/
Aldosterona
/
Músculo Liso Vascular
Limite:
Animals
Idioma:
En
Revista:
Am J Physiol
Ano de publicação:
1993
Tipo de documento:
Article