Mechanisms of Dexamethasone-Induced Hypertension

Ong, Sharon L.H.
Zhang, Yi
Whitworth, Judith A.

High Blood Pressure Research Unit, John Curtin School of Medical Research, Australian National University, Canberra, Australia

*Address correspondence to this author at the High Blood Pressure Research Unit, John Curtin School of Medical Research, Australian National University, PO Box 334, Canberra City 2601, Australian Capital Territory, Australia; Tel: 612-61252597; Fax: 612-61252337; E-mail: [email protected]

Received: 09 July, 2008 Revised: 29 July, 2008 Accepted: 15 August, 2008

Current Hypertension Reviews 5(1):p 61-74, 2009.

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 (DEX-HT) 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.