Background/Aim: Glucocorticoid activity is modulated by NADP(+)- and NAD(+)-dependent isoforms of the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta HSD) which convert glucocorticoids to their inactive metabolites. The NAD(+)-dependent isoform, 11 beta HDS2, is present in the distal nephron where it confers aldosterone specificity on mineralocorticoid receptors. The objective of this study was to establish whether renal 11 beta HSD activities are affected by changes in sodium and potassium balance and by metabolic acidosis. Methods: Renal 11 beta HSD activities were measured ex vivo from rats fed normal and high- and low-potassium diets and a low-sodium diet or given 1.5% NH4Cl to drink. Results: Rats maintained on high-potassium and low-sodium diets exhibited 59% (p < 0.01) and 28% (p < 0.05) decreases, respectively, in NAD(+)-dependent renal 11 beta HSD activity (relative to mts fed control diet) with no changes in NADP(+)-dependent cortisol oxidation. Short-term (3 day) and longer-term (10 day) metabolic acidosis also decreased NAD(+)-dependent 11 beta HSD activity by 50 and 52%, respectively, without affecting NADP(+)-dependent cortisol oxidation. The low-potassium diet had no detectable effect on renal 11 beta HSD activities. Conclusion: These results suggest that adaptations to a high-potassium or a low-sodium diet and to metabolic acidosis involve decreases in renal 11 beta HSD2 activity, enhancing the access of glucocorticoids to renal corticosteroid receptors, Copyright (C) 2000 S. Karger AG, Basel.
|Number of pages||8|
|Publication status||Published - 2000|