Inhibition by nicotine of the formation of prostacyclin-like activity in rabbit and human vascular tissue.
1 Rings of vascular tissue (from rabbit aorta or human peripheral vein) were incubated at room temperature in Tyrode solution in the absence or presence of nicotine or indomethacin. 2 Addition of portions of the incubates to human platelet-rich plasma (HPRP) elicited a decrease in adenosine 5'-diphosphate (ADP)-induced platelet aggregation in this plasma. Authentic prostacyclin (PGI2) also induced such a decrease. The decreased aggregation amplitudes that followed the addition of the vascular tissue incubates and of PGI2 were equally potentiated by theophylline (10(-4) M). 3 Both nicotine and indomethacin counteracted the formation of platelet anti-aggregatory activity in the vascular tissue incubates. The IC50S of nicotine and of indomethacin on the formation of platelet antiaggregatory activity were 2 X 10(-5) M and 6 X 10(-6) M, respectively. 4 Nicotine failed to affect the platelet anti-aggregatory effect induced by authentic PGI2 in HPRP. 5 It is concluded that nicotine counteracts the formation of platelet anti-aggregatory activity in rabbit aorta and human peripheral vein by eliciting an inhibitory effect on the bioformation of prostacyclin in these types of vascular tissue.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D001808:Blood Vessels / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009538:Nicotine / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000096:biosynthesis*; D011817:Rabbits; D013045:Species Specificity; D013806:Theophylline / Q000494:pharmacology
D011453:Prostaglandins; D000244:Adenosine Diphosphate; D009538:Nicotine; D013806:Theophylline; D011464:Epoprostenol; D007213:Indomethacin