Article date: February 1980
By: T. SONNENFELD, Å. WENNMALM in Volume 71, Issue 2, pages 609-613
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.
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 (10−4m).
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 times 10−5m and 6 times 10−6m, respectively.
Nicotine failed to affect the platelet anti‐aggregatory effect induced by authentic PGI2 in HPRP.
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.
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.
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 (10−4m).
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 times 10−5m and 6 times 10−6m, respectively.
Nicotine failed to affect the platelet anti‐aggregatory effect induced by authentic PGI2 in HPRP.
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.
DOI: 10.1111/j.1476-5381.1980.tb10980.x
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