Glucocorticoid-induced hypertension and the nitric oxide system

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.