Sulfur dioxide (SO₂) is a common exogenous atmospheric pollutant. Studies have shown that SO₂ can cause vasodilation as a gas signaling molecule, but the specific signaling pathways are not well understood. This study aimed to explore the underlying mechanism behind the effects of SO₂ on vasodilation of isolated rat aorta. The results showed that when the dose of SO₂ was 30 μM, the vasodilation of endothelium-intact rings was partially suppressed by LY294002 and N^G-nitro-l-arginine methyl ester, and the protein levels of phosphoinositide 3-kinase (PI3K), p-Akt, and p-endothelial nitric oxide synthase (p-eNOS) were significantly increased. When the dose of SO₂ was 300 μM or 1500 μM, the vasodilation of endothelium-denuded rings did not change after application of the inhibitor, but the protein levels of PI3K, p-Akt, and p-eNOS were significantly decreased, and the activity of NOS and the level of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) were significantly increased. We speculate that the mechanism of SO₂-induced vasodilatation likely involved the endothelial PI3K/Akt/eNOS and NO/cGMP signal pathways. In addition, at the concentration of 1500 μM, SO₂ markedly increased the level of caspase-3 and caspase-9. The results suggest that high concentrations of SO₂ may cause damage to blood vessels. This study will help to further inform the etiologies of SO₂-related cardiovascular disease.

二氧化硫（SO ₂）是一种常见的外源性大气污染物。研究表明，SO ₂可以作为一种气体信号分子引起血管舒张，但是具体的信号途径尚不清楚。这项研究旨在探讨SO ₂对离体大鼠主动脉血管舒张作用背后的潜在机制。结果表明，当SO ₂剂量为30μM时，LY294002和N ^G-硝基-1-精氨酸甲酯可部分抑制内皮完整环的血管舒张，磷酸肌醇3-激酶（PI3K）的蛋白水平受到抑制。，p-Akt和p-内皮一氧化氮合酶（p-eNOS）明显增加。当SO ₂的剂量为300μM或1500μM时，添加抑制剂后内皮剥脱环的血管舒张没有改变，但PI3K，p-Akt和p-eNOS的蛋白质水平显着降低，并且NOS的活性和一氧化氮（NO）和环鸟苷单磷酸（cGMP）的水平显着增加。我们推测，SO ₂诱导的血管舒张的机制可能与内皮PI3K / Akt / eNOS和NO / cGMP信号通路有关。此外，在1500μM的浓度下，SO ₂显着提高了caspase-3和caspase-9的水平。结果表明高浓度的SO ₂可能会损坏血管。这项研究将有助于进一步告知SO ₂相关心血管疾病的病因。