ABSTRACT
The present study was designed to investigate whether N-alpha-tosyl L-arginine methyl ester [TAME]-esterase activation could be the result of endothelial dysfunction. Thoracic aorta from rats was mounted in an organ bath containing Krebs solution. Intact and endothelium denuded aortic strips were challenged with different concentrations of TAME (10(-15)-10(-1) m). The effects of aspirin, a cyclo-oxygenase pathway inhibitor, were also studied on [TAME]-esterase induced contraction on rat aorta strips. Our results showed that aspirin definitely blocked TAME-esterase induced contractions on rat aortic strips. In conclusion, the present work supported the hypothesis that [TAME]-esterase induced contraction in rat aorta in vitro was mediated through release of prostaglandin(s) as a result of endothelial dysfunction.
