The vasorelaxant effect and its mechanisms of sodium bisulfite as a sulfur dioxide donor

To study the biological role of bisulfite on vascular contractility and its underlying cellular and molecular mechanisms, to explore whether bisulfite can be used as a sulfur dioxide (SO2) donor in the biological experiments, the vasorelaxant effects of sodium bisulfite and sodium sulfite on isolated rat thoracic aortic rings were compared: and the signal transduction pathways and the ion channels involved in the vascular effects of bisulfite were investigated. The results show that: (1) Sodium bisulfite relaxed rat thoracic aortic rings in a concentration-dependent manner (from 100 to 4000 mu M); however, sodium sulfite at 500 and 1000 mu M caused vasoconstriction, and only at higher concentrations (from 2000 to 4000 mu M) it caused vasorelaxation in a concentration-dependent manner. (2) The vasorelaxation caused by the bisulfite at low concentrations (<= 500 mu M) was endothelium-dependent, but at high concentrations (>= 1000 mu M) it was endothelium-independent. (3) The vasorelaxation by the bisulfite at the low concentrations was partially mediated by the cGMP pathway and the vasorelaxation was related to big-conductance Ca2+-activated K+ (BKCa) channel, but not due to prostaglandin, protein kinase C (PKC) and cAMP pathways. (4) The vasorelaxation by the bisulfite at high concentrations was partially inhibited by tetraethylammonium (TEA) and glibenclamide, suggesting that the vasorelaxation was related to ATP-sensitive K+ channel (K-ATP) and L-type calcium-channel. These results led to the conclusion that bisulfite (HSO3-) might be a vasoactive factor and sodium bisulfite can be used as a SO2 donor for the study of SO2 biology. (c) 2012 Elsevier Ltd. All rights reserved.