ArticleJournal of the American Society of Nephrology : JASN2008
A switch in the mechanism of hypertension in the syndrome of apparent mineralocorticoid excess.
Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed.
- Localisation of corticosteroids in male mouse kidney by mass spectrometry imaging.Journal of molecular endocrinology · 2026Article
- Pendrin is upregulated by corticosterone and participates in its pressor response.American journal of physiology. Renal physiology · 2026Article
- Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Loss of Adam10 Disrupts Ion Transport in Immortalized Kidney Collecting Duct Cells.Function (Oxford, England) · 2021Article
- Posaconazole-Induced Hypertension Masquerading as Congenital Adrenal Hyperplasia in a Child with Cystic Fibrosis.Case reports in medicine · 2020Article
- Unravelling drug-induced hypertension: molecular mechanisms of aldosterone-independent mineralocorticoid receptor activation by posaconazole.Clinical kidney journal · 2018Article
- 11β-Hydroxysteroid Dehydrogenases and Hypertension in the Metabolic Syndrome.Current hypertension reports · 2017Review
- ISN Forefronts Symposium 2015: The Evolution of Hypertension-Old Genes, New Concepts.Kidney international reports · 2016Article
- Dexamethasone and insulin activate serum and glucocorticoid-inducible kinase 1 (SGK1) via different molecular mechanisms in cortical collecting duct cells.Physiological reports · 2016Article
- Conditional Deletion of Hsd11b2 in the Brain Causes Salt Appetite and Hypertension.Circulation · 2016Article
- Vasodysfunction That Involves Renal Vasodysfunction, Not Abnormally Increased Renal Retention of Sodium, Accounts for the Initiation of Salt-Induced Hypertension.Circulation · 2016Review
- Mineralocorticoid Excess or Glucocorticoid Insufficiency: Renal and Metabolic Phenotypes in a Rat Hsd11b2 Knockout Model.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Hypertrophy in the Distal Convoluted Tubule of an 11β-Hydroxysteroid Dehydrogenase Type 2 Knockout Model.Journal of the American Society of Nephrology : JASN · 2015Article
- Pressure natriuresis and the renal control of arterial blood pressure.The Journal of physiology · 2014Review
- Glucocorticoids and renal Na+ transport: implications for hypertension and salt sensitivity.The Journal of physiology · 2014Review
- Acute inhibition of NCC does not activate distal electrogenic Na+ reabsorption or kaliuresis.American journal of physiology. Renal physiology · 2014Article
- Failure to downregulate the epithelial sodium channel causes salt sensitivity in Hsd11b2 heterozygote mice.Hypertension (Dallas, Tex. : 1979) · 2012Article
- A urine-concentrating defect in 11β-hydroxysteroid dehydrogenase type 2 null mice.American journal of physiology. Renal physiology · 2012Article
- Autonomic-immune-vascular interaction: an emerging concept for neurogenic hypertension.Hypertension (Dallas, Tex. : 1979) · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
The syndrome of apparent mineralocorticoid excess arises from nonfunctional mutations in 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2), an enzyme that inactivates cortisol and confers aldosterone specificity on the mineralocorticoid receptor. Loss of 11betaHSD2 permits glucocorticoids to activate the mineralocorticoid receptor, and the hypertension in the syndrome is presumed to arise from volume expansion secondary to renal sodium retention. An 11betaHSD2 null mouse was generated on an inbred C57BL/6J genetic background, allowing survival to adulthood. 11betaHSD2(-/-) mice had BP approximately 20 mmHg higher on average compared with wild-type mice but were volume contracted, not volume expanded as expected. Initially, impaired sodium excretion associated with increased activity of the epithelial sodium channel was observed. By 80 days of age, however, channel activity was abolished and 11betaHSD2(-/-) mice lost salt. Despite the natriuresis, hypertension remained but was not attributable to intrinsic vascular dysfunction. Instead, urinary catecholamine levels in 11betaHSD2(-/-) mice were double those in wild-type mice, and alpha1-adrenergic receptor blockade rescued the hypertensive phenotype, suggesting that vasoconstriction contributes to the sustained hypertension in this model. In summary, it is proposed that renal sodium retention remains a key event in apparent mineralocorticoid excess but that the accompanying hypertension changes from a renal to a vascular etiology over time.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.