SummaryThe acute effects of the angiotensin converting enzyme inhibitor captopril were studied in patients With essential (n = 9) or renovascular hypertension (n = 10) 75 min after ingestion of 25 mg of the drug, and 13 patients were restudied after 2 rnonths when on 150–600 mg/day. Captopril acutely decreased the arterial plasma angiotensin II (PA II) level by 49 % (P<0.001) with no further change during chronic treatment. Plasma aldosterone concentration dropped, while plasma renin activity and plasma angiotensin I levels rose during acute and chronic treatment. Mean brachial artery Pressure was acutely reduced by 16.4 mm Hg (P<0.001) while the chronic reduction was significantly greater by 9.2 mm Hg (P<0.001). A slight increase of heart rate of 3 beats/min (P<0.005) \vas observed in the acute but not in the chronic study.When compared with essential hypertension, patients with renovascular hypertension had a higher Control PRA level and a greater acute and chronic fall of blood pressure during captopril (P<0.05 for all), but the overlap was considerable. However, post-captopril plasma levels of angiotensin I Were highly significantly different between both•orms of hypertension and correcdy classified 9.5 % of the patients; minimal misclassification (5.3 %) was achieved by combining post-captopril angiotensin I with pre-captopril plasma angiotensin II levels.The data indicate that the hypotensive effect of Captopril is at least partly related to the changes of Arterial PA 11. The response of blood pressure to captopril does not allow a clear-cut distinction between essential and renovascular hypertension, but the components of the renin angiotensin system are more sensitive.