EFFECTS OF NICOTINE ON CARDIAC PROSTAGLANDIN AND PLATELET THROMBOXANE SYNTHESIS

Abstract

1 Rabbit hearts were perfused with a solution containing [¹⁴C]-arachidonic acid (AA) and various concentrations of nicotine (3 × 10⁻⁸ to 3 × 10⁻⁵m). The venous effluent was collected and extracted for lipid acid material, which was subsequently subjected to thin layer radiochromatography. 2 Human platelets were incubated with nicotine (10⁻⁸ to 10⁻⁴m), in the absence or presence of unlabelled AA. The amount of smooth muscle stimulating activity resulting from 30 s of incubation was tested on a rabbit aortic strip. 3 In hearts perfused with [¹⁴C]-AA; nicotine induced a dose-related depression of the release of [¹⁴C]-6-keto-prostaglandin F_1a, and a parallel increase in the release of [¹⁴C]-prostaglandin E₂. 4 Nicotine neither induced synthesis of thromboxane in human platelets, nor affected the platelet synthesis of thromboxane induced by AA. 5 It is suggested that nicotine affects the metabolism of prostaglandin endoperoxides in the heart by inhibiting their conversion to prostacyclin and facilitating, directly or indirectly, the formation of prostaglandin E₂.