Uridine 5′-triphosphate (UTP) has an important role as an extracellular signaling molecule that regulates inflammation, angiogenesis, and vascular tone. While chronic hypertension has been shown to promote alterations in arterial vascular tone regulation, carotid artery responses to UTP under hypertensive conditions have remained unclear. The present study investigated carotid artery responses to UTP 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 after pretreatment with phenylephrine, SHR exhibited significantly lower arterial relaxation responses compared with WKY. Moreover, UTP-induced relaxation was substantially reduced by endothelial denudation and by the nitric oxide (NO) synthase inhibitor N^G-nitro-L-arginine in both SHR and WKY. The difference in UTP-induced relaxation between both groups was abolished by the selective P2Y₂ receptor antagonist AR-C118925XX and the cyclooxygenase (COX) inhibitor indomethacin but not by the thromboxane-prostanoid receptor antagonist SQ29548. Furthermore, we detected the release of PGE₂, PGF_2α, 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.

尿苷 5'-三磷酸 (UTP) 作为调节炎症、血管生成和血管张力的细胞外信号分子具有重要作用。虽然慢性高血压已被证明会促进动脉血管张力调节的改变，但在高血压条件下颈动脉对 UTP 的反应仍不清楚。本研究调查了自发性高血压大鼠 (SHR) 和对照 Wistar 京都大鼠 (WKY) 的颈动脉对 UTP 的反应。因此，我们的结果发现，虽然 UTP 在用去氧肾上腺素预处理后促进来自 SHR 和 WKY 的分离颈动脉段的浓度依赖性松弛，但与 WKY 相比，SHR 表现出显着较低的动脉松弛反应。而且，SHR 和 WKY 中的^G-硝基-L-精氨酸。选择性 P2Y ₂受体拮抗剂 AR-C118925XX 和环氧合酶 (COX) 抑制剂吲哚美辛消除了两组之间 UTP 诱导的松弛的差异，但血栓烷-前列腺素受体拮抗剂 SQ29548 没有消除。此外，我们在基线和响应 UTP 时检测到SHR 和 WKY 颈动脉中 PGE ₂、PGF _2α和 PGI ₂的释放。UTP 给药也增加了 WKY 中的TXA ₂水平，但没有增加 SHR。总体而言，我们的结果表明 UTP 诱导的颈动脉松弛在 SHR 中受损，这可能是由于 P2Y ₂受损 受体信号传导、内皮 NO 减少和 COX 衍生的血管收缩剂前列腺素水平增加。