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      Effects of Changes in Dietary Intake of Sodium and Potassium and of Metabolic Acidosis on 11β-Hydroxysteroid Dehydrogenase Activities in Rat Kidney


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          Background/Aim: Glucocorticoid activity is modulated by NADP<sup>+</sup>- and NAD<sup>+</sup>-dependent isoforms of the enzyme 11β-hydroxysteroid dehydrogenase (11βHSD) which convert glucocorticoids to their inactive metabolites. The NAD<sup>+</sup>-dependent isoform, 11βHSD2, is present in the distal nephron where it confers aldosterone specificity on mineralocorticoid receptors. The objective of this study was to establish whether renal 11βHSD activities are affected by changes in sodium and potassium balance and by metabolic acidosis. Methods: Renal 11βHSD activities were measured ex vivo from rats fed normal and high- and low-potassium diets and a low-sodium diet or given 1.5% NH<sub>4</sub>Cl 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<sup>+</sup>-dependent renal 11βHSD activity (relative to rats fed control diet) with no changes in NADP<sup>+</sup>-dependent cortisol oxidation. Short-term (3 day) and longer-term (10 day) metabolic acidosis also decreased NAD<sup>+</sup>-dependent 11βHSD activity by 50 and 52%, respectively, without affecting NADP<sup>+</sup>-dependent cortisol oxidation. The low-potassium diet had no detectable effect on renal 11βHSD activities. Conclusion: These results suggest that adaptations to a high-potassium or a low-sodium diet and to metabolic acidosis involve decreases in renal 11βHSD2 activity, enhancing the access of glucocorticoids to renal corticosteroid receptors.

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          Most cited references4

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          Human hypertension caused by mutations in the kidney isozyme of 11 beta-hydroxysteroid dehydrogenase.

          The syndrome of apparent mineralocorticoid excess (AME) is an inherited form of human hypertension thought to result from a deficiency of 11 beta-hydroxysteroid dehydrogenase (11 beta HSD). This enzyme normally converts cortisol to inactive cortisone and is postulated to thus confer specificity for aldosterone upon the mineralocorticoid receptor. We have analysed the gene encoding the kidney isozyme of 11 beta HSD and found mutations on both alleles in nine of 11 AME patients (eight of nine kindreds). These mutations markedly affect enzymatic activity. They thus permit cortisol to occupy the renal mineralocorticoid receptor and thereby cause sodium retention and hypertension.
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            Cloning and tissue distribution of the human 1 lβ-hydroxysteroid dehydrogenase type 2 enzyme

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              • Abstract: not found
              • Article: not found

              Characterization of 11β-hydroxysteroid dehydrogenase of human placenta: Evidence for the existence of two species of 11β-hydroxysteroid dehydrogenase


                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                February 2000
                14 January 2000
                : 8
                : 1
                : 44-51
                aCentre for Nephrology, The Rayne Institute, Royal Free and University College Medical School, and bDepartment of Biochemistry and Molecular Biology, Royal Free and University College Medical School, London, UK
                20647 Exp Nephrol 2000;8:44–51
                © 2000 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 3, References: 29, Pages: 8
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/20647
                Self URI (text/html): https://www.karger.com/Article/FullText/20647
                Self URI (journal page): https://www.karger.com/SubjectArea/Nephrology
                Original Paper

                Cardiovascular Medicine,Nephrology
                Kidney,Potassium,Glucocorticoids,Sodium,11β-Hydroxysteroid dehydrogenase,Acid-base balance


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