Human platelet thromboxane synthesis is unaffected by nicotine

Summary. The effect of nicotine (2times 10‐7‐2times 10_4M) on arachidonate (AA)‐induced platelet aggregation and on the bioformation of thromboxane (TxB2) in human platelets was investigated. Human platelet‐rich plasma (HPRP) and human platelet suspension (HPS) were prepared from venous blood from donors who had not taken aspirin‐like drugs for at least one week. Using HPRP, nicotine was inefficient in blocking platelet aggregation from threshold AA concentrations–in contrast to indomethacin and aspirin–and also in prolonging the interval between the addition of A A and the initiation of aggregation. In other experiments, platelet microsomes prepared from HPS were incubated with 14C‐AA in the presence of nicotine, and the labelled metabolites were separated and quantified radiocbromatographically. Addition of nicotine to the incubations did not affect the amount of TxBa formed compared to controls; indomethacin, on the other hand, efficiently inhibited TxB2 formation as did pre‐treatment of the donors with aspirin. The results indicate that human platelet cyclo‐oxygenase, unlike, for example, rabbit renal cyclo‐oxygenase, is resistant to the inhibitory action of nicotine. The possible relevance of a tissue difference for tobacco smoking is pointed out.