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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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 SO(2) on vascular contractility and its level in vascular tissues, a vasodilation study of isolated rat thoracic aortic rings by gaseous SO(2) was carried out. The level of SO(2) in vascular tissue was assayed using a modified high-performance liquid chromatographic method with fluorescence detection (HPLC-FD). The results show that gaseous SO(2) (from 1 microM to 2000 microM) relaxed rat thoracic aortic rings in a dose-dependent manner. The physiological concentrations of SO(2) in thoracic aortic tissues and plasma in rats were 127.76 +/- 31.34 microM and 16.77+/-8.24 microM, respectively; The vasorelaxant effect of gaseous SO(2) at physiological and low concentrations (<450 microM) was endothelium dependent, and at high concentrations (>500 microM) was endothelium independent. The results also show that SO(2) could be endogenously generated in vascular tissues, and mainly in vascular endothelial cells; acetylcholine (Ach) increased the SO(2) level in vascular tissue, and noradrenaline (NE) decreased the SO(2) level. These findings demonstrate that gaseous SO(2) is a vasorelaxant substance, and the vasorelaxant effect of gaseous SO(2) is much stronger than that of its derivatives sulfite and bisulfite, which result from the inactivation process of SO(2) gas transmitter by which SO(2) is hydrated to form sulfite, and the latter is enzymatically oxidized to form sulfate. These findings also demonstrate that endogenous SO(2) level in vascular tissue may be regulated by Ach and NE.[1]


  1. Vasodilator effect of gaseous sulfur dioxide and regulation of its level by Ach in rat vascular tissues. Meng, Z., Li, J., Zhang, Q., Bai, W., Yang, Z., Zhao, Y., Wang, F. Inhal. Toxicol (2009) [Pubmed]
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