The influence of aprotinin as a kallidinogenase inactivator on the antihypertensive effect of angiotensin I converting enzyme inhibitor (CEI) was studied in two-kidneyed and one-clipped hypertensive rats. Sixteen two-kidneyed and one-clipped hypertensive rats and sham-operated normotensive rats were prepared for this experiment. They were divided into two groups: those with the aprotinin infusion and those without. The effects of the oral administration of CEI were compared as regards mean arterial pressure (MAP) and urinary kallikrein activity (UKA). In 8 hypertensive rats under glucose infusion, MAP fell from 184.4 ± 4.5 to 106.3 ± 5.2 mm Hg, and UKA changed from 1.37 ± 0.18 nkat/12h to 0.61 ± 0.11 nkat/12h after the administration of CEI. In the remaining hypertensive rats under aprotinin infusion, MAP decreased from 175.0 ± 3.0 to 140.6 ± 5.1 mm Hg, and UKA slightly changed from 0.72 ± 0.25 nkat/12 h to 0.59 ± 0.12 nkat/12 h. Thus, the decrease of MAP after the administration of CEI was suppressed by the aprotinin infusion, and this significant difference was supported by the decrease of UKA. As for 16 normotensive rats, CEI did not alter MAP, nor did aprotinin have any effect on it. However, UKA tended to decrease after the administration of CEI. These results suggest that both the kallikreinkinin system and the renin-angiotensin system play an important role in the maintenance of high blood pressure in two-kidneyed and one-clipped chronically hypertensi