The effect on contraction-relaxation mechanism ofclopidogrel in rat aorta

As a thienopridine derivation clopidogrel is an inactive prodrug which inhibate adenosine diphosphate induced trombosite aggregation. Clopidogrel used in reduction of atherotrombotic events, in stroke, myocardial infarction and in treatment of cardiovasculer diseases. Furthermore it is observed that it reduces stent retrombosis after percutaneous coronary intervention. In this study potential effects of clopidogrel on aort contractions of 12-14 week 300-350 gr weight male winstar rats was researched. In the study by using isolated organ bath, potential effects of non cumulative 10 nM and 100 nM doses of clopidogrel on conraction-relaxation mechanism of rat aorta was tested. As a result of study we observed that while clopidogrel dose independently statisticaly significantly inhibite fenilefrin induced contraction of rat aorta with 10 nM and 100 nM doses (more significantly with 10 nM dose). With application of sodium nitroprusside which cause endothel independent relaxation on rat aorta, clopidogrel dose-dependently had no effect at 10 nM dose while it facilitated relaxation statistically significantly at 100 nM dose (p<0.05). When we applied acetylcholine which cause endothel dependent relaxation on rat aorta clopidogrel dose indepently facilitated relaxation statisticaly significantly at 10 nM dose (p<0.05) while it had no effect at 100 nM dose. With findings obtained as a result of study we observed that clopidogrel dose-independently inhibite contractions of rat aorta and when relaxation protochol was examined it was observed that clopidogrel facilitate relaxation both endothel dependently and independently. Due to these effects of clopidogrel on rat aorta it gives rise to the thought that with further studies except its usage in clinical treatment as an anti-aggregan it may have antihipertansive effects. ,Key words: Clopidogrel, aorta, contraction, relaxation, rat.