Vasodilator effect of gaseous sulfur dioxide and regulation of its level by Ach in rat vascular tissues

To explore the toxicological and physiological role of gaseous SO₂ on vascular contractility and its level in vascular tissues, a vasodilation study of isolated rat thoracic aortic rings by gaseous SO₂ was carried out. The level of SO₂ in vascular tissue was assayed using a modified high-performance liquid chromatographic method with fluorescence detection (HPLC-FD). The results show that gaseous SO₂ (from 1?μM to 2000?μM) relaxed rat thoracic aortic rings in a dose-dependent manner. The physiological concentrations of SO₂ in thoracic aortic tissues and plasma in rats were 127.76?±?31.34?μM and 16.77±8.24?μM, respectively; The vasorelaxant effect of gaseous SO₂ at physiological and low concentrations (<450?μM) was endothelium dependent, and at high concentrations (>500?μM) was endothelium independent. The results also show that SO₂ could be endogenously generated in vascular tissues, and mainly in vascular endothelial cells; acetylcholine (Ach) increased the SO₂ level in vascular tissue, and noradrenaline (NE) decreased the SO₂ level. These findings demonstrate that gaseous SO₂ is a vasorelaxant substance, and the vasorelaxant effect of gaseous SO₂ is much stronger than that of its derivatives sulfite and bisulfite, which result from the inactivation process of SO₂ gas transmitter by which SO₂ is hydrated to form sulfite, and the latter is enzymatically oxidized to form sulfate. These findings also demonstrate that endogenous SO₂ level in vascular tissue may be regulated by Ach and NE.