Enhancement of PGI2 formation by a new vasodilator, 2-nicotinamidoethyl nitrate in the coupled system of platelets and aortic microsomes

Exogenous arachidonate addition to the coupled system of platelets and aortic microsomes resulted in production of TXA₂ and PGI₂ (detected as the stable degradation products, TXB₂ and 6-keto PGF_1α, respectively). Imidazole, papaverine and dipyridamole increased PGI₂ and decreased TXA₂ in the coupled system. All of these agents inhibited TXA₂ formation by platelets from arachidonate. Nitroglycerin did not show any effect on PGI₂ and TXA₂ formation in the coupled system and on TXA₂ formation by platelets. In contrast with these compounds, in spite of showing no inhibitory effect on TXA₂ formation by platelets alone, 2-nicotinamidoethyl nitrate (SG-75) increased PGI₂ and decreased TXA₂ in the coupled system. It is suggested that SG-75 accelerated the conversion of PGH₂ to PGI₂ so that smaller amounts of TXA₂ was produced in the coupled system.