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Coexpression of Mineralocorticoid Receptors and 11ß-Hydroxysteroid Dehydrogenase 2 in Human Gastric Mucosa

The Departments of Medicine III (K.K., S.O., H.S., T.S., T.T.) and Pathology (H.S., S.M., H.N.), Tohoku University School of Medicine, Sendai, Japan; The Department of Medicine III (T.M., K.Y.), Gifu University School of Medicine, Gifu, Japan; Baker Medical Research Institute (Z.K.), Melbourne, Australia

Address all correspondence and requests for reprints to: Katsuaki Kato, M.D., the Department of Internal Medicine (III), Tohoku University School of Medicine, 1-1 Seiryomachi, Aoba-ku, Sendai 980, Japan. E-mail: kato-ka{at}mx2.nisiq.net

The role of mineralocorticoids in human gastrointestinal tract is well established. In the stomach, aldosterone is thought to regulate electrolyte transport associated with gastric acid secretion. In mineralocorticoid target organs, the action of the glucocorticoid inactivating enzyme 11ß-hydroxysteroid dehydrogenase type 2 (11ß-HSD2) facilitates aldosterone binding to a nonselective mineralocorticoid receptor (MR) in the face of high levels of circulating glucocorticoids. In the present study, we examined 25 specimens of human stomach for the presence of MR and 11ß-HSD2 using a [³H]aldosterone binding assay, Northern blot analysis, RT-PCR, and immunohistochemistry. Specific [³H]aldosterone binding sites were detected in gastric fundic mucosa, but not in the antrum. In fundic mucosa the K_d was 0.72 ± 0.05 nmol/L (mean ± SE), and B_max was 6.0 ± 1.4 fmol per milligram of protein. Northern blot analysis demonstrated a faint band for MR mRNA at 6.0 kb, although message for 11ß-HSD2 was undetectable. However, RT-PCR demonstrated specific PCR products for both MR and 11ß-HSD2. Immunohistochemistry demonstrated the colocalization of MR and 11ß-HSD2 only in parietal cells. MR-positive cells were further characterized by electron microscopy, confirming the identity of parietal cells. This study shows that parietal cells contain both MR and 11ß-HSD2, suggesting that the human stomach is a novel target organ for mineralocorticoids. Aldosterone may, therefore, regulate biological functions of parietal cells including gastric acid secretion.

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