The aim of this study was to investigate whether total stenosis of the common carotid artery (ipsilateral) would affect the vascular responsiveness of the contralateral carotid as well as the basilar artery from guinea pigs. With this purpose, the carotid artery was occluded with a silk thread at a position close to its origin. Vascular reactivity experiments using standard muscle bath were performed 7, 15, 30, and 90 days after carotid occlusion. Stenosis induced a progressive reduction in the contraction induced by endothelin-1, phenylephrine and KCl in the ipsilateral carotid, when compared to their respective age-matched SHAM groups. Endothelial removal or incubation of endothelium-intact ipsilateral carotids with L-NAME, a nitric oxide synthase inhibitor, did not alter the response to endothelin-1 or phenylephrine, when compared to the endothelium-intact ipsilateral carotid in the absence of the inhibitor. Interestingly, an increased contractile response to endothelin-1, phenylephrine and KCl was observed in the contralateral carotid. Indomethacin, a non-selective cyclooxygenase inhibitor, prevented the increased contraction to endothelin-1 in the contralateral carotid. Stenosis also induced an increase in the contractile response to endothelin-1 in the basilar artery while the contractile response to phenylephrine and KCl were reduced. Indomethacin, but not L-NAME, prevented the increased contraction to endothelin-1 in the basilar artery. Morphometric analysis showed no differences in the medial area (wall thickness) of carotid or basilar arteries from the stenosis group when compared to their respective age-matched SHAM groups. The present study confirms the importance of adaptation to stenosis on the vascular reactivity of the stenosed artery to different vasoconstrictor agents. Moreover, our results show that stenosis induces alterations of the vascular reactivity on arteries distant from the site of injury. The increased response to endothelin-1 in the contralateral carotid artery and basilar artery seems to involve the release of vasoconstrictor prostanoids from endothelial origin.