Uridine triphosphate (UTP) and uridine diphosphate (UDP) play an important role as extracellular signalling molecules that regulates various function including angiogenesis and vascular tone. Although chronic arterial hypertension has been shown to promote alterations in arterial vascular tone regulation, carotid arterial responses to UTP and UDP under hypertensive conditions has remained unclear. The present study investigated carotid arterial responses to UTP and UDP in spontaneously hypertensive rats (SHR) and control Wistar Kyoto rats (WKY). Accordingly, our results found that although UTP promotes concentration-dependent relaxation in isolated carotid artery segments from both SHR and WKY precontracted with phenylephrine, SHR exhibited significantly lower arterial relaxation responses compared to WKY. On the other hand, UDP elicited slight relaxation at intermediate concentrations and contraction at higher concentrations in the carotid arteries of SHR and WKY. Accordingly, UDP-induced responses were similar in both groups. UTP-induced relaxation was substantially reduced by endothelial denudation and by the nitric oxide (NO) synthase inhibitor in both SHR and WKY. The difference in UTP-induced relaxation between both groups was abolished by the selective P2Y₂ receptor antagonist and the cyclooxygenase (COX) inhibitor but not by the thromboxane-prostanoid receptor antagonist. Furthermore, we detected the release of PGE₂, PGF_2a, and PGI₂ in the carotid arteries of SHR and WKY, both at baseline and in response to UTP. UTP administration also increased TXA₂ levels in WKY but not SHR. Overall, our results suggest that UTP-induced relaxation in carotid arteries is impaired in SHR perhaps due to impaired P2Y₂ receptor signaling, reductions in endothelial NO, and increases in the levels of COX-derived vasoconstrictor prostanoids.