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Effect of nicotine on the formation of prostacyclin‐like activity and thromboxane in rabbit aorta and platelets
Author(s) -
Alster Pawel,
Wennmalm Åke
Publication year - 1984
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.1476-5381.1984.tb10743.x
Subject(s) - prostacyclin , platelet , aorta , arachidonic acid , thromboxane , chemistry , nicotine , microsome , prostaglandin , thromboxane a2 , biochemistry , medicine , enzyme
1 The effect of nicotine on the bioformation of prostacyclin (PGI 2 ) and of thromboxane (Tx)B 2 in rabbit aorta and platelets, respectively, was investigated. 2 Rabbit aortic rings were incubated with [ 14 C]‐arachidonic acid ([ 14 C]‐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 [ 14 C]‐AA and the products formed were separated with t.l.c. 3 Rings of aorta were found to be incapable of converting added [ 14 C]‐AA to labelled 6‐keto‐PGF 1α (the stable hydrolysis product of PGI 2 ). Rings of aorta incubated in saline medium spontaneously formed PGI 2 ‐like activity. This formation was dose‐dependently inhibited by nicotine, with an I 50 of about 10 −4 m . 4 Platelet microsomes converted [ 14 C]‐AA to labelled TxB 2 . This formation was unaffected by nicotine. 5 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.