Abstract
In spontaneously hypertensive rats (SHR), the hypotensive effect of captopril (30 mg/kg/day per os for 4 days), which inhibits the converting enzyme when given orally, was significantly potentiated rather than suppressed by aprotinin (100, 000 KlU/day s.c. for 7 days), but was not affected by indomethacin. These findings suggest that neither the kallikrein-kinin system nor the prostaglandin system is involved in any of the hypotensive actions of captopril in SHR other than the inhibition of the converting enzyme.