Vasodilator effect of gaseous sulfur dioxide and regulation of its level by Ach in rat vascular tissues
Authors: Meng, Ziqiang; Li, Junling; Zhang, Quanxi; Bai, Weiming; Yang, Zhenhua; Zhao, Ying; Wang, Faqi
Source: Inhalation Toxicology, Volume 21, Number 14, December 2009 , pp. 1223-1228(6)
Publisher: Informa Healthcare
Abstract: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.
Document Type: Research article
Publication date: 2009-12-01