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

Edwards, C. R. W.; Burt, D.; McIntyre, Margaret; Kloet, E. Ronald de; Stewart, Paul M.; Brett, L; Sutanto, W.; Monder, Carl

doi:10.1016/s0140-6736(88)90742-8

Cited by 1,013 publications

(429 citation statements)

References 21 publications

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“…Aldosterone specificity can also be conferred to MRs by the enzyme 1 l fl-hydroxysteroid dehydrogenase (11fl-OHSD; Edwards et al, 1988;Funder et al. 1988).…”

Section: Receptor Specificity Conferring Mechanismsmentioning

confidence: 99%

“…The biological significance of this converting enzyme for the aldosterone selective binding in the kidney was revealed in animals that were pretreated with the licorice component glycyrrhizic acid, a blocker of I lfl-OHSD. In the presence of this blocker, corticosterone was not metabolized and binds to MRs like aldosterone {Funder et Edwards et al, 1988).…”

Section: Receptor Specificity Conferring Mechanismsmentioning

confidence: 99%

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Mineralocorticoid and glucocorticoid receptors in the brain. Implications for ion permeability and transmitter systems

Joëls

Kloet

1994

Progress in Neurobiology

367

168

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“…Aldosterone specificity can also be conferred to MRs by the enzyme 1 l fl-hydroxysteroid dehydrogenase (11fl-OHSD; Edwards et al, 1988;Funder et al. 1988).…”

Section: Receptor Specificity Conferring Mechanismsmentioning

confidence: 99%

Section: Receptor Specificity Conferring Mechanismsmentioning

confidence: 99%

Mineralocorticoid and glucocorticoid receptors in the brain. Implications for ion permeability and transmitter systems

Joëls

Kloet

1994

Progress in Neurobiology

367

168

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“…1 However, the enzyme 11␤-hydroxysteroid dehydrogenase type 2 (11BHSD2) protects the mineralocorticoid receptor from the mineralocorticoid actions of cortisol by converting cortisol to cortisone. [2][3][4] Cortisone has a low affinity for the mineralocorticoid receptor 5,6 and aldosterone is therefore the major mineralocorticoid in vivo. The 11BHSD2 gene is located on chromosome 16q22 7 and is expressed at high levels in the kidney, colon and placenta.…”

Section: Introductionmentioning

confidence: 99%

Association between a variant in the 11β-hydroxysteroid dehydrogenase type 2 gene and primary hypertension

et al. 2000

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The enzyme 11␤-hydroxysteroid dehydrogenase type 2 (11BHSD2) converts cortisol to cortisone in the kidney, thereby protecting the mineralocorticoid receptor from the mineralocorticoid actions of cortisol. The syndrome of Apparent Mineralocorticoid Excess (AME), a rare monogenic form of early onset hypertension with autosomal recessive inheritance, is caused by homozygous or compound heterozygous loss of function mutations in the 11BHSD2 gene. Association has been reported between a microsatellite marker flanking the 11BHSD2 gene (D16S496) and primary hypertension. The aim of this study was to identify variants in the 11BHSD2 gene and to test if such variants or the D16S496 are associated with primary hypertension, in Swedes. To address this, the coding sequences of the 11BHSD2 gene was screened for mutations in 20 patients with primary hypertension with single strand conformation polymorphism and direct DNA sequencing techniques. A poly-

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“…AME had provided us with a unique experiment of biology; here was an example of severe mineralocorticoid excess caused by cortisol itself, suggesting that 11␤-HSD may play a crucial role in normal physiology in dictating MR specificity. Subsequently this was shown to be the case; 11␤-HSD inactivates cortisol to cortisone in the mineralocorticoid target tissues, kidney, colon and salivary gland permitting aldo to interact with the MR. 52,53 In AME or following liquorice ingestion, this does not occur and cortisol can then act as a potent mineralocorticoid.…”

Section: Liddle's Syndromementioning

confidence: 99%

Monogenic forms of mineralocorticoid hypertension: insights into the pathogenesis of ‘essential’ hypertension?

Petrelli

Stewart

1998

J Hum Hypertens

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Hypertension is a common condition, which, depending on its definition, affects 10-25% of the population. Because it is an established risk factor for coronary and cerebrovascular disease, hypertension has, quite rightly, been targeted as an important factor in determining the health of the nation. Despite this we can explain the underlying cause of a patient's hypertension in Ͻ5% of cases; the remainder are labelled 'essential' hypertension, an elegant way of stating that the aetiology is unknown. As a result, in the vast majority of cases treatment is given on an empirical basis.In the last 5 years, significant advances have been made in our understanding of the pathogenesis of hypertension with the characterisation of three forms of inherited hypertension. All arise because of distinct, single gene mutations but can result in the same phenotype, that of mineralocorticoid hypertension. The purpose of this article is to review these 'monogenic' forms of mineralocorticoid hypertension, glucocorticoid-remediable hyperaldosteronism, Liddle's syndrome and apparent mineralocorticoid excess, and to discuss their significance to the broader population with essential hypertension.Glucocorticoid remediable aldosteronism (GRA) (also referred to as dexamethasone suppressible hyperaldosteronism or glucocorticoidsuppressible hyperaldosteronism)In 1966 a hypertensive father and son were described with a new disorder that mimicked priCorrespondence: PM Stewart, Professor

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

Cited by 1,013 publications

References 21 publications

Mineralocorticoid and glucocorticoid receptors in the brain. Implications for ion permeability and transmitter systems

Mineralocorticoid and glucocorticoid receptors in the brain. Implications for ion permeability and transmitter systems

Association between a variant in the 11β-hydroxysteroid dehydrogenase type 2 gene and primary hypertension

Monogenic forms of mineralocorticoid hypertension: insights into the pathogenesis of ‘essential’ hypertension?

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