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Renal 11β-hydroxysteroid dehydrogenases (11β-HSDs) are subject to modulation by various endogenous factors. 11β-HSDs convert glucocorticoids into inactive 11-ketones and thereby determine tissue levels of active glucocorticoids and thus the extent of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) activation. As such, modulation of the activity of renal 11β-HSDs may contribute to...
Glucocorticoid access to renal corticosteroid receptors is regulated by 11β-hydroxysteroid dehydrogenases (11β-HSDs), converting 11β-hydroxyglucocorticoids into inactive 11-ketones. This mechanism plays a key role in maintaining normal salt-water homeostasis and blood pressure. To study whether renal cortical proximal and distal tubular 11β-HSDs are modulated, upon shifting the electrolyte status...
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