Effect of nicotine on the formation of prostacyclin-like activity and thromboxane in rabbit aorta and platelets.

The effect of nicotine on the bioformation of prostacyclin (PGI2) and of thromboxane (Tx)B2 in rabbit aorta and platelets, respectively, was investigated. Rabbit aortic rings were incubated with [14C]-arachidonic acid ( [14C]-AA) and the incubation products were separated with thin layer chromatography (t.l.c.). Alternatively, the aortic rings were incubated without substrate and their spontaneous formation of platelet anti-aggregatory activity was measured. Rabbit platelet microsomes were incubated with [14C]-AA and the products formed were separated with t.l.c. Rings of aorta were found to be incapable of converting added [14C]-AA to labelled 6-keto-PGF1 alpha (the stable hydrolysis product of PGI2). Rings of aorta incubated in saline medium spontaneously formed PGI2-like activity. This formation was dose-dependently inhibited by nicotine, with an I50 of about 10(-4) M. Platelet microsomes converted [14C]-AA to labelled TxB2. This formation was unaffected by nicotine. It is concluded that a true difference in sensitivity to nicotine exists between cyclo-oxygenase in rabbit aorta and platelets. The data also demonstrate a tissue difference between rabbit aorta and platelets concerning their utilization of exogenous AA as substrate in the formation of platelet active compounds.