Nitric oxide complements prostacyclin in the regulation of endothelial thromboresistance under flow conditions.
Using a novel method of measuring thrombogenesis on the surface of rabbit aorta endothelium superfused with whole blood, it was demonstrated that the thrombogenic properties of endothelium are potentiated by pretreatment with inhibitors of nitric oxide (NO) synthase (NG-monomethyl-L-arginine, MeArg, 100 mcM) or cyclooxygenase (aspirin, ASA, 60 mcM). Since MeArg is less effective than aspirin and moreover does not influence thrombogenesis after previous inhibition of the synthesis of PGI2, it is concluded that the generation of NO by vascular endothelium complements PGI2 in its antithrombotic activity but NO may be ineffective when the generation of PGI2 has been impaired.
Korbut
R
R
Department of Pharmacology, Nicolaus Copernicus University School of Medicine, Cracow, Poland.
Ocetkiewicz
A
A
Gryglewski
R J
RJ
D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology; D004730:Endothelium, Vascular / Q000187:drug effects*; D011464:Epoprostenol / Q000097:blood*; D066298:In Vitro Techniques; D009569:Nitric Oxide / Q000097:blood*; D019335:Nitroarginine; D011817:Rabbits; D013927:Thrombosis / Q000097:blood / Q000517:prevention & control*
D019335:Nitroarginine; D009569:Nitric Oxide; D001120:Arginine; D011464:Epoprostenol; D001241:Aspirin