Glucocorticoid hormones, both naturally occurring and synthetic, have long been recognized as a major cause of hypertension. There are well-described experimental models of glucocorticoid-induced hypertension, such as adrenocorticotropic hormone- and dexamethasone-induced hypertension in rats, although the exact mechanism of glucocorticoid-induced hypertension remains unclear. It was initially considered to be due to mineralocorticoid receptor activation but more recent studies have not supported this notion. Current evidence demonstrates the importance of the nitric oxide (NO) system and interactions between NO and reactive oxygen species in the development of glucocorticoid-induced hypertension. This review highlights the pathways contributing to NO deficiency, which encompass the availability of l-arginine, endothelial NO synthase function and the extent of NO inactivation during oxidative stress.
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http://dx.doi.org/10.1586/eem.12.19 | DOI Listing |
J Clin Med
November 2024
Department of Nephrology and Renal Transplantation, Medical School, National and Kapodistrian University of Athens, Laiko Hospital, 11527 Athens, Greece.
Eur J Endocrinol
November 2024
Department of Internal Medicine I, Division of Endocrinology and Diabetes, University Hospital, University of Würzburg, 97080 Würzburg, Germany.
Objective: Cushing's syndrome (CS) results in increased cardiovascular (CV) morbidity and mortality. Subtype-specific differences and possible reversibility after biochemical cure are not well investigated.
Design: Prospective cohort study evaluating the CV status in different forms of endogenous cortisol excess.
Methods Mol Biol
October 2024
Gavin Herbert Eye Institute-Center for Translational Vision Research, Department of Ophthalmology, Department of Physiology and Biophysics, University of California Irvine School of Medicine, Irvine, California, USA.
FASEB J
August 2024
Department of Ophthalmology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Glucocorticoid use may cause elevated intraocular pressure, leading to the development of glucocorticoid-induced glaucoma (GIG). However, the mechanism of GIG development remains incompletely understood. In this study, we subjected primary human trabecular meshwork cells (TMCs) and mice to dexamethasone treatment to mimic glucocorticoid exposure.
View Article and Find Full Text PDFCurr Eye Res
December 2024
Department of Ophthalmology, University Eye Hospital, Hannover Medical School, Hannover, Germany.
Purpose: This study aimed to assess the effectiveness of monocular and bilateral injections of Dexamethasone-21-acetate (Dex-21-Ac) into the murine fornix twice a week as a glucocorticoid-induced ocular hypertension model and investigated potential systemic side effects.
Methods: Dex-21-Ac was administered twice weekly in three groups: bilateral injections, monocular injections, and a control group receiving the vehicle solution bilateral. After 21 days, enucleated eyes were examined using immunocytochemistry (ICC), and organ histology was performed.
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