Mechanisms of Dexamethasone-Induced Hypertension

被引:18
|
作者
Ong, Sharon L. H. [1 ]
Zhang, Yi [1 ]
Whitworth, Judith A. [1 ]
机构
[1] Australian Natl Univ, John Curtin Sch Med Res, High Blood Pressure Res Unit, POB 334, Canberra, ACT 2601, Australia
基金
英国医学研究理事会;
关键词
Dexamethasone-induced hypertension; glucocorticoid; nitric oxide; oxidative stress; pathogenesis; reactive oxygen species;
D O I
10.2174/157340209787314315
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
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.
引用
收藏
页码:61 / 74
页数:14
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