Glucocorticoid excess is associated with hypertension in man and in animals. This type of hypertension is of rapid onset and independent of salt intake; it can be inhibited by glucocorticoid antagonists, such as RU486. In normal rats, RU486 blunts vascular reactivity to norepinephrine and angiotensin II . In normal rats on low-salt diet, it induces a fall in blood pressure of approximately 20 mm Hg, due to decreased vascular resistance. This suggests that in some conditions, endogenous glucocorticoids contribute to the maintenance of blood pressure by enhancing vascular reactivity.