The vasodilator effect and its mechanism of sulfur dioxide-derivatives on isolated aortic rings of rats

The vasodilator effect of exogenous sulfur dioxide (SO2) derivatives (mixture of sodium bisulfite and sodium sulfite, 3:1 M/M in neutral solution) on rat vascular system was studied in order to explore the mechanism of blood pressure lowered by SO2 and its derivatives. Isolated rat aortic rings were perfused in bath tubes containing various chemicals and their tensions were recorded. The results showed: (1) The SO2 derivatives could relax isolated aorta precontracted by norepinephrine ( NE) or potassium chloride (KCl) in a dose-dependent manner. (2) This vasodilator effect was attenuated after preincubation with indomethacin, but was not affected by N-L-nitro-arginine, methylene blue, and propranolol, and was independent of the aorta endothelium. (3) The vasoconstriction responses induced by NE, KCl, or Ca2+ were antagonized by SO2 derivatives in a noncompetitive manner. (4) The vasoconstrictions of two components (initial fast vasoconstriction induced by intracellular Ca2+ release and sustained vasoconstriction evoked by extracellular Ca2+ influx) were also inhibited by SO2 derivatives. These results led to the conclusions: The SO2 derivatives could cause vasorelaxation by a direct role of the chemicals on aortic smooth muscle cells. It was not dependent on vascular endothelium and was independent of nitric oxide (NO). It is suggested that SO2 and its derivatives might be also vasoactive substances that modulate changes of blood pressure, like other gasotransmitters. The vasorelaxation might be related to the inhibition effects of SO2 derivatives on Ca2+ entry through both potential-dependent calcium channels and receptor-operating calcium channels, and also to the inhibition of intracellular Ca2+ release. The vasorelaxation was at partly related to the increase of prostacyclin (PGI(2)) induced by SO2 derivatives.