[Effects pf captopril and D-penicillamine on kinins-mediated and chronic inflammation].
In our study the effects of angiotension converting enzyme inhibitor captopril and immunosuppressant agent d-penicillamine were investigated on inflammations mediated by kinins and on adjuvant arthritis in rat paw oedema tests. Kinins mediated inflammations were increased by small doses of captopril (0.04-5 mg/kg per os) in a dose dependent manner. However this effect of captopril was reduced at higher doses of the drug (5-400 mg/kg). In the case of d-penicillamine there was exerted an inflammation increasing effect similarly to captopril. Maximum value of this action could be measured at dose 100 mg/kg per os. After administration higher doses of d-penicillamine were not revealed any depression in inflammation increasing effect. In capillary resistance studies we have shown capillary resistance increasing action of captopril that was dose depend. However this effect was not found in the case of d-penicillamine. According to these finding kinins mediated inflammation increasing effects of captopril and d-penicillamine are suggested as a results of their ability inhibit angiotensin converting enzyme. Maximum depression at higher doses of captopril may be caused by its capillary resistance elevating action. In chronic inflammations studies we have shown developments of secondary symptoms of adjuvant arthritis inhibiting effects of captopril and d-penicillamine in a dose dependent manner. We assume that immunosuppressive action of both drug are responsible for reduction of chronic inflammations. Our study strengthens the argument that captopril can be used in therapy of rheumatoid arthritis. Further clinicopharmacological studies of captopril may clarify the role of this drug in therapy of rheumatoid diseases.
Gáspár
R
R
Szent-Györgyi Albert Orvostudományi Egyetem Gyógyszerhatástani Intézet, Szeged.
Blazsó
G
G
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001169:Arthritis, Experimental / Q000276:immunology*; D001920:Bradykinin / Q000494:pharmacology; D002196:Capillaries / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology; D002216:Captopril / Q000494:pharmacology*; D003907:Dexamethasone / Q000494:pharmacology; D004487:Edema; D007166:Immunosuppressive Agents / Q000494:pharmacology; D007705:Kinins / Q000494:pharmacology*; D010396:Penicillamine / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014655:Vascular Resistance / Q000187:drug effects
D000806:Angiotensin-Converting Enzyme Inhibitors; D007166:Immunosuppressive Agents; D007705:Kinins; D003907:Dexamethasone; D002216:Captopril; D010396:Penicillamine; D001920:Bradykinin
Kaptopril és d-penicillamin hatása a kinin mediált, illetve krónikus gyulladásra.