ArticleProceedings of the National Academy of Sciences of the United States of America1999
Down-regulation of the expression of endothelial NO synthase is likely to contribute to glucocorticoid-mediated hypertension.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.
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Who cites it
79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 287 citations in OpenAlex.
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- The hypertension of Cushing's syndrome: controversies in the pathophysiology and focus on cardiovascular complications.Journal of hypertension · 2015Pooled it
- Acute hydrocortisone administration reduces cardiovagal baroreflex sensitivity and heart rate variability in young men.The Journal of physiology · 2018Trial
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- Social Isolation, Loneliness and Subclinical Atherosclerosis.Current atherosclerosis reports · 2026Review
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- The Impact of Stress on the Functioning and Survival of Transplanted Kidneys-Biological Mechanisms, Clinical Implications, and Therapeutic Perspectives.International journal of molecular sciences · 2025Review
- Baxdrostat: A Next-Generation Aldosterone Synthase Inhibitor Offering New Hope in Resistant Hypertension.Biomolecules · 2025Review
- Negative association between serum calcium and glucocorticoid-induced hypertension in thyroid-associated ophthalmopathy patients treated with methylprednisolone.Frontiers in endocrinology · 2025Article
- Health position paper and redox perspectives - Disease burden by transportation noise.Redox biology · 2024Review
- Metabolomic Profiling of Hormonal Contraceptive Use in Young Females Using a Commercially Available LC-MS/MS Kit.Metabolites · 2023Article
- Endothelial Cell Response in Kawasaki Disease and Multisystem Inflammatory Syndrome in Children.International journal of molecular sciences · 2023Article
- Combined Statin and Glucocorticoid Therapy for the Safer Treatment of Preterm Birth.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Living Alone Increases the Risk of Hypertension in Older Chinese Adults: A Population-Based Longitudinal Study.Innovation in aging · 2023Article
- The sex-dependent response to psychosocial stress and ischaemic heart disease.Frontiers in cardiovascular medicine · 2023Review
- Cerebral Blood Flow in Predator Stress-Resilient and -Susceptible Rats and Mechanisms of Resilience.International journal of molecular sciences · 2022Article
- Transportation noise pollution and cardiovascular disease.Nature reviews. Cardiology · 2021Review
- Glucocorticoids: Fuelling the Fire of Atherosclerosis or Therapeutic Extinguishers?International journal of molecular sciences · 2021Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertension is a side effect of systemically administered glucocorticoids, but the underlying molecular mechanism remains poorly understood. Ingestion of dexamethasone by rats telemetrically instrumented increased blood pressure progressively over 7 days. Plasma concentrations of Na(+) and K(+) and urinary Na(+) and K(+) excretion remained constant, excluding a mineralocorticoid-mediated mechanism. Plasma NO(2)(-)/NO(3)(-) (the oxidation products of NO) decreased to 40%, and the expression of endothelial NO synthase (NOS III) was found down-regulated in the aorta and several other tissues of glucocorticoid-treated rats. The vasodilator response of resistance arterioles was tested by intravital microscopy in the mouse dorsal skinfold chamber model. Dexamethasone treatment significantly attenuated the relaxation to the endothelium-dependent vasodilator acetylcholine, but not to the endothelium-independent vasodilator S-nitroso-N-acetyl-D,L-penicillamine. Incubation of human umbilical vein endothelial cells, EA.hy 926 cells, or bovine aortic endothelial cells with several glucocorticoids reduced NOS III mRNA and protein expression to 60-70% of control, an effect that was prevented by the glucocorticoid receptor antagonist mifepristone. Glucocorticoids decreased NOS III mRNA stability and reduced the activity of the human NOS III promoter (3.5 kilobases) to approximately 70% by decreasing the binding activity of the essential transcription factor GATA. The expressional down-regulation of endothelial NOS III may contribute to the hypertension caused by glucocorticoids.
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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.