Inhibition of vascular permeability changes in rats by captopril.
Systemic treatment of rats with captopril (50 mg/kg body wt per os), a specific competitive inhibitor of angiotensin l-converting enzyme, significantly inhibits vascular permeability changes induced by the intradermal injection of the vasoactive mediators histamine, bradykinin, serotonin, and compound 48/80. This effect of captopril is both dose- and time-dependent with approximately 60% inhibition of edema formation observed 7 h after captopril treatment (100 mg/kg body wt per os). The inhibitory effect of captopril on edema formation is temporally unrelated to the inhibition of serum angiotensin l-converting enzyme activity or serum prostaglandin E2 levels and is not inhibited by systemic treatment of rats with indomethacin. The data suggest that captopril may have potent antiinflammatory activity through as yet undefined mechanisms.
D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D002199:Capillary Permeability / Q000187:drug effects*; D002216:Captopril / Q000494:pharmacology*; D015237:Dinoprost; D015232:Dinoprostone; D004305:Dose-Response Relationship, Drug; D004487:Edema / Q000139:chemically induced; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D011392:Proline / Q000031:analogs & derivatives*; D011458:Prostaglandins E / Q000097:blood; D011460:Prostaglandins F / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains; D012867:Skin / Q000098:blood supply; D013929:Thromboxane B2 / Q000097:blood
D011458:Prostaglandins E; D011460:Prostaglandins F; D013929:Thromboxane B2; D011392:Proline; D002216:Captopril; D015237:Dinoprost; D007703:Peptidyl-Dipeptidase A; D015232:Dinoprostone; D001920:Bradykinin