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Journal ArticleDOI

Cloning and tissue distribution of the human 1 lβ-hydroxysteroid dehydrogenase type 2 enzyme

TLDR
The 11β-hydroxysteroid dehydrogenase (11βHSD) as mentioned in this paper was found to protect the nonselective mineralocorticoid receptor from occupation by glucocorticity, and to modulate access of glucoc Corticoid to glucoc corticoid receptors resulting in protection of the fetus and gonads.
About
This article is published in Molecular and Cellular Endocrinology.The article was published on 1994-11-01. It has received 678 citations till now. The article focuses on the topics: Glucocorticoid receptor & Apparent mineralocorticoid excess syndrome.

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Citations
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Journal ArticleDOI

Hormonal Regulation of Glucocorticoid Inactivation and Reactivation in αT3-1 and LβT2 Gonadotroph Cells.

TL;DR: Gonadotroph 11βHSD enzyme activity can act to regulate local glucocorticoid availability to mediate the influence of the HPA axis on gonadotrophic function.
Journal ArticleDOI

ACTH Infusion Impairs Baroreflex Sensitivity-Implications for Cardiovascular Hypoglycemia-Associated Autonomic Failure.

TL;DR: Investigate the role of the adrenocorticotropin hormone (ACTH)-adrenal axis in decreasing BRS and the possibility that hypoglycemia-induced increases in ACTH may contribute to the cardiovascular component of HAAF.
Journal ArticleDOI

The hypertensiogenetic steroid 19-nor-progesterone does not influence cortisol inactivation by 11beta-hydroxysteroid dehydrogenase type 2

TL;DR: In conclusion, 19-nor-P did not inhibit human 11β-HSD2 and seems not to be involved in human hypertension, but may be converted by extra-adrenal tissues into 19- Nor-deoxycorticosterone (DOC) or 19-Nor-cortICosterone, which are potent mineralocorticoids and may be involved In the pathogenesis of hypertension during pregnancy.
Journal ArticleDOI

Hipertensión arterial mineralocorticoidea

TL;DR: De otra parte, defectos congenitos o adquiridos en the enzima 11β-Hidroxiesteroide deshidrogenasa tipo 2 resultan en una ineficiente inactivacion de cortisol a cortisona favoreciendo la aparicion de hipertension por activacion del receptor mineralocorticoideo.
Book ChapterDOI

Molecular Genomics of Mineralocorticoid Action

TL;DR: The mineralocorticoid receptor is a member of the nuclear receptor superfamily that acts as a ligand-dependent transcription factor that mediates its effects not only through a transcriptional mechanism but also through nongenomic mechanisms and perhaps through transrepression.
References
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Journal ArticleDOI

Mineralocorticoid action: target tissue specificity is enzyme, not receptor, mediated

TL;DR: The presence of the enzyme 11 beta-hydroxy-steroid dehydrogenase, which converts cortisol and corticosterone, but not aldosterone, to their 11-keto analogs, means that these analogs cannot bind to mineralocorticoid receptors.
Journal ArticleDOI

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

TL;DR: Findings seem to explain why sodium retention, hypokalaemia, and hypertension develop in subjects with congenital deficiency of 11 beta-OHSD and those in whom the enzyme has been inhibited by liquorice.
Journal ArticleDOI

A workbench for multiple alignment construction and analysis.

TL;DR: An interactive program, MACAW (Multiple Alignment Construction and Analysis Workbench), that allows the user to construct multiple alignments by locating, analyzing, editing, and combining “blocks” of aligned sequence segments.
Journal ArticleDOI

Mineralocorticoid activity of liquorice: 11-beta-hydroxysteroid dehydrogenase deficiency comes of age

TL;DR: It is suggested that in both conditions there is a defect in the renal conversion of cortisol to cortisone by 11 beta-OHSD which results in high intrarenal cortisol levels, acting on type 1 mineralocorticoid receptors to cause sodium retention.
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