We have previously shown that ACTH administration (1 mg/day) for 5 days raises systolic blood pressure (BP) by some 20 mmHg in both normotensive and hypertensive subjects, accompanied by hypokalaemia, urinary Na retention, a rise in fasting blood glucose and a fall in plasma renin concentration (PRC). In the present study cortisol and deoxycorticosterone (DOC) were infused for 5 days in 7 and 6 subjects respectively at rates appropriate for conditions of ACTH stimulation to determine whether the effects of ACTH could be reproduced by either steroid. Cortisol infusion increased systolic BP from a control of 108 +/- 7 mmHg to 129 +/- 7 mmHg on day 5, p less than 0.001. Plasma [Na] increased from 137 +/- 1 to 139 +/- 1 mmol/l (p less than 0.01), plasma [K] fell from 3.8 +/- 0.1 to 3.6 +/- 0.1 mmol/l (p less than 0.05); blood glucose rose from 3.9 +/- 0.2 to 4.7 +/- 0.2 mmol/l (p less than 0.001); PRC fell from 26 +/- 7 to 12 +/- 3 mu iu /ml (p less than 0.05); renin substrate rose from 1629 +/- 140 to 2206 +/- 453 pmol AI/ml, (p less than 0.05); urine Na excretion fell from 93 +/- 19 to 41 +/- 10 mmol on day 2 (p less than 0.05) and rose to 209 +/- 31 mmol 48 hrs after infusion (p less than 0.001); urine output rose from 2.0 +/- 0.35 to 2.89 +/- 0.46 L on day 5, (p less than 0.01). Plasma cortisol levels were similar to those seen with ACTH treatment. DOC infusion was associated with a fall in diastolic BP (control 64.2 +/- 4.0 mmHg, day 5 57.0 +/- 4.2 mmHg, p less than 0.01). Urine Na excretion fell from 77 +/- 12 mmol/day to 49 +/- 8 mmol/day on day 1, (p = 0.06) and body weight rose from 76.0 +/- 5.8 kg to 76.8 +/- 5.9 kg day 5 (p less than 0.001). Thus in man, cortisol infusion (in contrast to DOC) at rates appropriate for conditions of ACTH stimulation reproduces both the BP and metabolic effects of ACTH. Whether cortisol acts to raise blood pressure by a classical glucocorticoid mechanism or by a hypertensinogenic mechanism is not known.