1. Captopril (25 mg) reduced plasma angiotensin II (ANG II) by 53% (P < 0·001) and mean brachial artery pressure (MBAP) by 18·7 mmHg (P < 0·001) within 75 min in 26 hypertensive patients. After 2 months (on 150–600 mg/day) MBAP had decreased by 27·1 mmHg (n = 18) with no further change of plasma ANG II. δMBAP was significantly related to control log plasma renin (PRA) and log ANG II in both conditions. 2. The acute depressor response to captopril was 11·2 mmHg greater (P < 0·001) than δMBAP during saralasin infusion (n = 12). 3. Heart rate slightly increased after acute administration of captopril (+ 3·3 beats/min; P < 0·005), but cardiac output was not significantly affected; systemic vascular resistance decreased by 10% (P < 0·01) with unchanged pulmonary vascular resistance. 4. During chronic administration, oxygen consumption, cardiac output and stroke volume increased by 15% (P < 0·01), with unchanged heart rate; systemic vascular resistance had dropped by 30% (P < 0·001). 5. Plasma ANG II and plasma aldosterone decreased, and PRA and ANG I increased acutely, with no further changes during chronic treatment.