It is well recognized that alterations on wall shear stress plays an important role on the development of atherosclerosis disease. It is known that oscillatory shear stress (OSS) flow pattern induces endothelial dysfunction via changes on nitric oxide (NO) pathway. NO is a potent vasodilator molecule and its availability can be evaluated by vasoreactivity organ chamber experiment. Arginase is an enzyme which is implicated in the signaling pathway of NO as it competes with endothelium nitric oxide synthase (eNOS) for the use of arginine. Increase in arginase expression and activity has been associated atherosclerosis, however the modulation of arginase by wall shear stress has never been studied before. This project consists of experimental work to better understand the implication of shear stress, NO and arginase expression in endothelial dysfunction of arteries. By using western blot and immunohistochemistry techniques we investigated the expression and localization of arginase in pig carotid arteries (PCA) perfused in an ex vivo arterial support system. While arginase I isoform was not present in PCA, arginase II was constitutively expressed. Its expression was augmented by exposure to high shear stress (HSS) flow and dependent of flow duration. OSS flow significantly increases the expression of arginase as compared to HSS. Inhibition of arginase in PCA perfused under OSS was not able to improve endothelial function neither NO availability. In a second part we characterize the geometry of rabbit carotid bifurcation and investigate if the receptor-mediated endothelial function and NO availability varies in this bifurcation. In the presence of NOS inhibitor, the contraction of the arteries in response to norepinephirne was higher. This difference is significant for segments which have the better endothelial dependant relaxation: the external carotid and the middle part of the common carotid.