Premium
EFFECTS OF NICOTINE ON CARDIAC PROSTAGLANDIN AND PLATELET THROMBOXANE SYNTHESIS
Author(s) -
WENNMALM AKE
Publication year - 1978
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1978.tb17318.x
Subject(s) - prostacyclin , nicotine , arachidonic acid , chemistry , platelet , thromboxane , medicine , prostaglandin , endocrinology , prostaglandin e2 , thromboxane b2 , prostaglandin h2 , thromboxane a synthase , thromboxane a2 , pharmacology , biochemistry , enzyme
1 Rabbit hearts were perfused with a solution containing [ 14 C]‐arachidonic acid (AA) and various concentrations of nicotine (3 × 10 −8 to 3 × 10 −5 m ). 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 −4 m ), 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 [ 14 C]‐AA; nicotine induced a dose‐related depression of the release of [ 14 C]‐6‐keto‐prostaglandin F 1a , and a parallel increase in the release of [ 14 C]‐prostaglandin E 2 . 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 E 2 .