ArticleHypertension (Dallas, Tex. : 1979)2011
Hsd11b2 haploinsufficiency in mice causes salt sensitivity of blood pressure.
Article in Hypertension (Dallas, Tex. : 1979), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 45 citations in OpenAlex.
- Upregulated Renal Mineralocorticoid Receptor and 11β-Hydroxysteroid Dehydrogenase Type 2 Are Associated with KInternational journal of molecular sciences · 2026Article
- High salt intake activates the hypothalamic-pituitary-adrenal axis, amplifies the stress response, and alters tissue glucocorticoid exposure in mice.Cardiovascular research · 2023Article
- Apparent mineralocorticoid excess: comprehensive overview of molecular genetics.Journal of translational medicine · 2022Review
- Activation of the Sympathetic Nervous System Promotes Blood Pressure Salt-Sensitivity in C57BL6/J Mice.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Relationship between the renin-angiotensin-aldosterone system and renal Kir5.1 channels.Clinical science (London, England : 1979) · 2019Article
- Animal Models of Hypertension: A Scientific Statement From the American Heart Association.Hypertension (Dallas, Tex. : 1979) · 2019Review
- Renal and Blood Pressure Response to a High-Salt Diet in Mice With Reduced Global Expression of the Glucocorticoid Receptor.Frontiers in physiology · 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
- 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
- Variants of 11β-hydroxysteroid dehydrogenase (HSD11B) gene type 1 and 2 in Chinese obese adolescents.Journal of endocrinological investigation · 2014Article
- Glucocorticoids and renal Na+ transport: implications for hypertension and salt sensitivity.The Journal of physiology · 2014Review
- Evidence for glucocorticoid-mediated hypertension after uninephrectomy.Physiological reports · 2013Article
- 11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action.Physiological reviews · 2013Review
- 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
- Regulation of transport in the connecting tubule and cortical collecting duct.Comprehensive Physiology · 2012Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Salt sensitivity of blood pressure is an independent risk factor for cardiovascular morbidity. Mechanistically, abnormal mineralocorticoid action and subclinical renal impairment may blunt the natriuretic response to high sodium intake, causing blood pressure to rise. 11β-Hydroxysteroid dehydrogenase type 2 (11βHSD2) controls ligand access to the mineralocorticoid receptor, and ablation of the enzyme causes severe hypertension. Polymorphisms in HSD11B2 are associated with salt sensitivity of blood pressure in normotensives. In this study, we used mice heterozygote for a null mutation in Hsd11b2 (Hsd11b2(+/-)) to define the mechanisms linking reduced enzyme activity to salt sensitivity of blood pressure. A high-sodium diet caused a rapid and sustained increase in blood pressure in Hsd11b2(+/-) mice but not in wild-type littermates. During the adaptation to high-sodium diet, heterozygotes displayed impaired sodium excretion, a transient positive sodium balance, and hypokalemia. After 21 days of high-sodium feeding, Hsd11b2(+/-) mice had an increased heart weight. Mineralocorticoid receptor antagonism partially prevented the increase in heart weight but not the increase in blood pressure. Glucocorticoid receptor antagonism prevented the rise in blood pressure. In Hsd11b2(+/-) mice, high-sodium feeding caused suppression of aldosterone and a moderate but sustained increase in corticosterone. This study demonstrates an inverse relationship among 11βHSD2 activity, heart weight, and blood pressure in a clinically important context. Reduced activity causes salt sensitivity of blood pressure, but this does not reflect illicit activation of mineralocorticoid receptors by glucocorticoids. Instead, we have identified a novel interaction among 11βHSD2, dietary salt, and circulating glucocorticoids.
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