Abstract
The comparative effects of nicotine and cotinine on the biosynthesis of prostacyclin (PGI 2) and thromboxane A 2 (TXA 2) in the horse aorta and platelet microsomes were studied. TXB 2 and 6-keto PGF1a stable metabolites of TXA 2 and PGI 2 respectively were determined by radioimmunoassay. TXA 2 production in the presence of either nicotine or cotinine treatment was not altered. However, a dose dependent inhibition of PGI 2 biosynthesis, and a dose dependent stimulation of PGI 2 biosynthesis, was observed in the presence of nicotine and cotinine respectively. Moreover, cotinine (10 b3 M) was able to prevent the inhibitory effect of nicotine on PGI 2 synthetase when preincubated with horse aorta microsomes. It appears that cotinine, the major nicotine metabolite resulting from a breakdown process, could be useful for the organism, at least for the cardiovascular system.
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