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      Renal 11-Beta-Hydroxysteroid Dehydrogenase: A Mechanism Ensuring Mineralocorticoid Specificity

      Hormone Research in Paediatrics

      S. Karger AG

      Mineralocorticoids, Glucocorticoids, Receptors, 11β-Hydroxysteroid dehydrogenase

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          In vitro studies with mineralocorticoid receptors (MR) have shown that they are non-specific and do not distinguish between glucocorticoids (cortisol in man, corticosterone in rodents) and aldosterone. These findings contrast with in vivo aldosterone selectivity. Our studies on the congenital deficiency of the enzyme 11β-hydroxysteroid dehydrogenase (11β-OHSD; which converts cortisol to cortisone or corticosterone to 11-dehydrocorticosterone) and acquired deficiency secondary to liquorice or carbenoxolone indicate that this enzyme plays a crucial role in protecting the MR from glucocorticoid exposure. The localisation of 11β-OHSD in both the proximal and distal nephron suggests that it has both an autocrine and a paracrine role. The presence of this protective mechanism in the toad bladder suggests that it is at least 300 million years old.

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          Author and article information

          Horm Res Paediatr
          Hormone Research in Paediatrics
          S. Karger AG
          02 December 2008
          : 34
          : 3-4
          : 114-117
          Department of Medicine, Western General Hospital, Edinburgh, UK
          181808 Horm Res 1990;34:114–117
          © 1990 S. Karger AG, Basel

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          Page count
          Pages: 4
          Hormonal Control of Arterial Pressure and Water Electrolyte Metabolism


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