Abstract
Hypertension is a well-recognized complication of excess glucocorticoids, both naturally-occurring and synthetic. Dexamethasone is a potent synthetic glucocorticoid, which has widespread clinical applications. As dexamethasone has purely glucocorticoid activity with negligible mineralocorticoid effects, dexamethasone-induced hypertension (DEXHT) models have been used for studying the mechanisms of glucocorticoid-induced hypertension. This review examines the characteristics and mechanisms of DEX-HT, both in the human and experimental animal models. The roles of hemodynamics, volume, renin-angiotensin-aldosterone system, sympathetic nervous system, vasodilators including nitric oxide, vasoconstrictors and reactive oxygen species in the pathogenesis of DEX-HT are reviewed and differences from hypertension due to naturally occurring steroids discussed.
Keywords: Dexamethasone-induced hypertension, glucocorticoid, nitric oxide, oxidative stress, pathogenesis, reactive oxygen species
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