It is generally believed that adrenal steroid hypertension is due to the 'mineralocorticoid' and/or 'glucocorticoid' activities of the steroid(s). The present study examines the blood pressure and metabolic effects of steroid hormone infusion in intact conscious sheep to assess the relative contributions of 'glucocorticoid' and 'mineralocorticoid' activity. Cortisol at 5 mg/h increased mean arterial pressure (MAP) but the effect was small (MAP + 10 mm Hg on day 5). This rate of infusion produces blood cortisol levels appropriate for maximal ACTH stimulation. Cortisol at 20 mg/hr produced hypertension (MAP + 25 mm Hg on day 5, p less than 0.01) but also produced the 'mineralocorticoid' effect of severe hypokalaemia. Dexamethasone at 1 mg/hr produced small increases in MAP but a profound fall in plasma [K]. Aldosterone at 80 microgram/hr (a pharmacological rate) produced hypokalaemia, urinary Na retention but no effect on MAP over 5 days. Thus, in short term infusion experiments, 'mineralocorticoid' effects are not associated with hypertension. Pharmacological concentrations of predominantly 'gluc-corticoid' steroid hormones produced hypertension but also exhibited substantial 'mineralocorticoid' activity. At levels approximating maximal physiological secretion, the rise in blood pressure was small. These results supported the contention that ACTH induced hypertension in sheep represents a mechanism different from a simple 'mineralocorticoid' or 'glucocorticoid' action.