The enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) plays a major role in the protection of the mineralocorticoid receptor (MR). This cellular mechanism of aldosterone selectivity relies on the coexpression of MR and 11 beta-OHSD in the same cells. Localization of renal 11 beta-OHSD along the nephron is reviewed; comparison of data contained in different species is made; and original data is presented to show that the catalytic activity of the enzyme in tubules from human kidney is the highest in the mineralocorticoid-sensitive distal nephron.
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Expression cloning of the aldosterone target cell-specific 11 beta-hydroxysteroid dehydrogenase from rabbit collecting duct cells.
Endocrinology
June 1995
Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA.
11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) is thought to confer aldosterone specificity to mineralocorticoid target cells by protecting the mineralocorticoid receptor from occupancy by endogenous glucocorticoids. We have recently described a novel isoform of 11-OHSD in the renal aldosterone target cells (11 beta-OHSD/CD) that differs from the previously characterized isoform (11 beta-OHSD-1). Unlike 11-OHSD-1, the collecting duct enzyme catalyzes irreversible dehydrogenation, has a very high affinity for its substrate, and is tissue-specific.
View Article and Find Full Text PDF11 beta-Hydroxysteroid dehydrogenase in renal collecting duct cells.
Steroids
February 1994
Department of Physiology, Dartmouth Medical School, Lebanon, NH 03756.
The purpose of this paper it to briefly review recent work from our laboratory dealing with the form of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) present in renal aldosterone target cells. It is well established that aldosterone is the physiological mineralocorticoid hormone. The observation that mineralocorticoid receptors have equal affinity for aldosterone and endogenous glucocorticoids, coupled with the fact that circulating levels of glucocorticoids are much higher than those of aldosterone, raises the question of how aldosterone can fulfill its function.
View Article and Find Full Text PDFExpression of 11 beta-OHSD along the nephron of mammals and humans.
Steroids
February 1994
INSERM U246, UER Xavier Bichat, Paris, France.
The enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) plays a major role in the protection of the mineralocorticoid receptor (MR). This cellular mechanism of aldosterone selectivity relies on the coexpression of MR and 11 beta-OHSD in the same cells. Localization of renal 11 beta-OHSD along the nephron is reviewed; comparison of data contained in different species is made; and original data is presented to show that the catalytic activity of the enzyme in tubules from human kidney is the highest in the mineralocorticoid-sensitive distal nephron.
View Article and Find Full Text PDFMinealocorticoid receptors and 11 beta-steroid dehydrogenase activity in renal principal and intercalated cells.
Am J Physiol
January 1994
Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire 03756.
Aldosterone exerts complex effects on the cortical collecting duct (CCD): it increases Na+ and K+ transport, and it also influences H+ and HCO3 transport. Whether these latter effects represent direct action of aldosterone on intercalated cells (ICC) or are secondary to changes in the transport of other electrolytes is unclear. Because the presence of specific receptors is the prerequisite of a direct steroid action, and mineralocorticoid receptors (MR) have not yet been demonstrated in ICC, in this study we determined the density of MR directly in isolated principal cells (PC) and beta-ICC.
View Article and Find Full Text PDFRenal handling of prednisolone/prednisone: effect of steroid dose and 11 beta-hydroxysteroid dehydrogenase.
Nephrol Dial Transplant
March 1995
Division of Nephrology, University Hospital of Berne, Switzerland.
Unlabelled: The purposes of this study were: (1) to determine under steady-state conditions whether the renal clearance of prednisolone is concentration dependent, and (2) to establish whether the urinary excretion of prednisolone and its biologically inactive 11-dehydro metabolite prednisone depend upon the activity of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD). For that purpose 10 healthy volunteers were infused to steady state over a 13-h period either at a low (11 micrograms/h x kg) or a high (70 micrograms/h x kg) rate with prednisolone on two occasions, once without and once with administration of glycyrrhetinic acid, an inhibitor of 11 beta-OHSD. Prednisolone and prednisone were measured by high-pressure liquid chromatography.
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