Release of prostaglandin I 2-like activity from the rat aorta: Effect of captopril, furosemide, and sodium

Abstract

The effect of captopril, furosemide, indomethacine and intake of sodium on the production of PGI 2-like material was studied in the rat aorta. Release of PGI 2-like material from these vessels was estimated by its ability to inhibit ADP-induced vessels was estimated by its ability to inhibit ADP-induced platelet aggregation. Pretreatment with indomethacin (15 mg/kg/day) reduced the capacity of the aorta to release PGI 2-like material. Pretreatment with captopril (10 mg/kg/day) had no effect. Intravenous furosemide (60 μg/ml plasma volume) increased the capacity of the aorta to inhibit by 28% (p<.025). The inhibitory capacity of aorta removed from rats on a low sodium diet did not differ from those on a high sodium diet. We conclude that the action of furosemide in reducing vascular tone may be related to stimulation of PGI 2 synthesis in blood vessels whereas the effect of captopril and sodiumin in reducing vascular tone may involve a mechanism unrelated to PGI 2 synthesis or may involve the synthesis of a prostaglandin other than PGI 2.