LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR

@article{Edwards1988LOCALISATIONO1,
  title={LOCALISATION OF 11$\beta$-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR},
  author={Christopher R. W. Edwards and D. Burt and M. A. Mcintyre and E. Ronald de Kloet and P. M. Stewart and L P Brett and W. S. Sutanto and Carl Monder},
  journal={The Lancet},
  year={1988},
  volume={332},
  pages={986-989}
}
11 beta-Hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess.
TLDR
Mutations in the HSD11B2 (HSD11K) gene encoding the kidney isozyme of 11-HSD have been detected in all kindreds with AME studied thus far, and this gene represents a candidate locus for the common, "essential" form of hypertension.
The 11β-Hydroxysteroid Dehydrogenase System, A Determinant of Glucocorticoid and Mineralocorticoid Action
TLDR
11β-HSD provide an important control of glucocorticoid action at a cellular level, and may represent new targets for therapeutic intervention.
The cortisol-cortisone shuttle and the apparent specificity of glucocorticoid and mineralocorticoid receptors
  • C. Edwards, P. Stewart
  • Medicine, Biology
    The Journal of Steroid Biochemistry and Molecular Biology
  • 1991
11β-Hydroxysteroid dehydrogenase in human vascular cells
TLDR
Results show that vascular 11βHSD activity could influence blood pressure without invoking renal sodium retention, and may indicate that impaired dehydrogenase activity in vascular wall results in increased vascular tone by the contribution of cortisol, which acts as a mineralocorticoid.
Coexpression of mineralocorticoid receptors and 11beta-hydroxysteroid dehydrogenase 2 in human gastric mucosa.
TLDR
Parietal cells contain both MR and 11beta-HSD2, suggesting that the human stomach is a novel target organ for mineralocorticoids, which may regulate biological functions of parietal cells including gastric acid secretion.
Localization of 11 beta-hydroxysteroid dehydrogenase: specific protector of the mineralocorticoid receptor in mammalian olfactory mucosa.
TLDR
The presence of a dehydrogenase activity separate from the nicotineamide-adenine dinucleotide phosphate (NADP)-dependent 11 beta HSD in the mammalian olfactory mucosa suggests that mineralocorticoid receptors present in acinar cells and sustentacular cells are aldosterone selective.
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References

SHOWING 1-10 OF 39 REFERENCES
Renal mineralocorticoid receptors and hippocampal corticosterone-binding species have identical intrinsic steroid specificity.
  • Z. Krozowski, J. Funder
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 1983
TLDR
It is suggested that hippocampal [3H]corticosterone-binding sites and renal MR may have identical intrinsic specificity for steroids, with apparent specificity differences the result of tissue-specific sequestration of naturally occurring steroids other than Aldo.
Syndrome of apparent mineralocorticoid excess. A defect in the cortisol-cortisone shuttle.
TLDR
It is suggested that cortisol acts as a potent mineralocorticoid in 11 beta-OHSD deficiency, which results in high intrarenal cortisol concentrations that then bind to the type I receptor.
Extravascular CBG-like sites in rat kidney and mineralocorticoid receptor specificity.
TLDR
It is proposed that extravascular CBG confers mineralocorticoid specificity on the papilla-inner medulla [3H]aldosterone binding sites and a countercurrent exchange model is proposed for renewable sequestration of corticosterone in the region.
Mineralocorticoid specificity of renal type I receptors: in vivo binding studies.
TLDR
Data are interpreted as evidence for a mechanism unrelated to extravascular CBG conferring mineralocorticoid specificity on renal type I receptors and two models derived from the findings consistent with such differential selectivity are proposed.
A syndrome of apparent mineralocorticoid excess associated with defects in the peripheral metabolism of cortisol.
TLDR
The decrease in the MCR permitted the maintenance of normal cortisol plasma levels and normal glucocorticoid function at a diminished rate of secretion, and serves as a biochemical marker of this hypertensive syndrome.
Metabolic and blood pressure responses to hydrocortisone in the syndrome of apparent mineralocorticoid excess.
TLDR
It is suggested that an abnormality in cortisol action or metabolism causing cortisol to behave as a potent mineralocorticoid may account for this syndrome of apparent mineraloc Corticoid excess.
Corticosterone binding sites along the rat nephron.
TLDR
The apparent maximal binding capacity of the cortical collecting tubule for corticosterone exceeded by nearly two orders of magnitude that of aldosterone previously measured by us in this structure, which is in agreement with the observations of other investigators in kidney cytosol.
Aldosterone binding in isolated tubules. III. Autoradiography along the rat nephron.
TLDR
Aldosterone binding was investigated along the nephron of adrenalectomized Wistar rats and it was concluded that the CCT and DCT present the highest binding capacity for aldosterone.
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