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INHIBITION BY NICOTINE OF THE FORMATION OF PROSTACYCLIN‐LIKE ACTIVITY IN RABBIT AND HUMAN VASCULAR TISSUE
Author(s) -
SONNENFELD T.,
WENNMALM Å.
Publication year - 1980
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.1476-5381.1980.tb10980.x
Subject(s) - prostacyclin , nicotine , platelet , chemistry , vascular tissue , theophylline , adenosine diphosphate , platelet aggregation , adenosine , pharmacology , blood vessel , aorta , medicine , endocrinology , biochemistry , biology , botany
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 (PGI 2 ) also induced such a decrease. The decreased aggregation amplitudes that followed the addition of the vascular tissue incubates and of PGI 2 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 IC 50 s of nicotine and of indomethacin on the formation of platelet antiaggregatory activity were 2 times 10 −5 m and 6 times 10 −6 m , respectively. 4 Nicotine failed to affect the platelet anti‐aggregatory effect induced by authentic PGI 2 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.