title: Prostacyclin, nitric oxide, and atherosclerosis.
abstract: Disorders in arterial production of PGI2 and NO occur in atherosclerosis. Exogenous PGI2 and NO are capable of interacting pharmacologically. We claim that no such direct interactions occur between endogenous endothelial PGI2 and NO. Studying mechanisms of cardiac reactive hyperemia in guinea pigs and of thrombolysis in cats, we surmise that in vivo vascular intima releases PGI2 intraluminally while NO is secreted abluminally and thus these two ephemeral mediators do not see each other. Hence, in any disease, the disturbances in endothelial generation of PGI2 or NO have to be scrutinized separately. It may well be that endogenous PGI2 maintains endothelial thromboresistance while NO controls arterial myocytes and tissues in which microcirculation is embedded. These responsibilities remain unshared. Interactions between PGI2 and NO are confined to pharmacological domains.
authors.affiliation: Department of Pharmacology, Medical College of Jagiellonian University, Cracow, Poland.
authors.forename: R J
authors.initials: RJ
authors.lastname: Gryglewski
authors.forename: S
authors.initials: S
authors.lastname: Chłopicki
authors.forename: J
authors.initials: J
authors.lastname: Swies
authors.forename: P
authors.initials: P
authors.lastname: Niezabitowski
mesh_terms: D000818:Animals; D001161:Arteriosclerosis / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects; D002415:Cats; D003327:Coronary Disease / Q000503:physiopathology; D006152:Cyclic GMP / Q000378:metabolism; D011464:Epoprostenol / Q000378:metabolism*; D006168:Guinea Pigs; D006940:Hyperemia / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D013927:Thrombosis / Q000378:metabolism; D013929:Thromboxane B2 / Q000378:metabolism
chemical_list: D009569:Nitric Oxide; D013929:Thromboxane B2; D011464:Epoprostenol; D006152:Cyclic GMP