Abstract
Despite many previous studies, the mechanism of glucocorticoid-induced hypertension remains unknown. The present review will introduce the results of our studies on this subject in patients with Cushing's syndrome and in experimental animals. Our studies indicate that the following multiple factors are involved in glucocorticoid-induced hypertension in humans and animals: 1) activation of the renin-angiotensin (R-A) system due to an increase in plasma renin substrate (PRS); 2) reduced activity of depressor systems, including the kallikrein-kinin (K-K) system, prostaglandins (PGs), and the endothelium-derived relaxing factor nitric oxide (NO); and 3) increased pressor responses to angiotensin II (Ang II) and norepinephrine. Furthermore, our in vitro studies have revealed that the number of Ang II type 1 receptors of vascular smooth muscle cells (VSMCs) is significantly increased by glucocorticoids. It is concluded that the pathogenesis of glucocorticoid-induced hypertension is multi-factorial, involving the various mechanisms described above.
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