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

The vasodilator effect of exogenous sulfur dioxide (SO(2)) 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 SO(2) 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 SO(2) 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 Ca(2+) were antagonized by SO(2) derivatives in a noncompetitive manner. (4) The vasoconstrictions of two components (initial fast vasoconstriction induced by intracellular Ca(2+) release and sustained vasoconstriction evoked by extracellular Ca(2+) influx) were also inhibited by SO(2) derivatives. These results led to the conclusions: The SO(2) 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 SO(2) 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 SO(2) derivatives on Ca(2+) entry through both potential-dependent calcium channels and receptor-operating calcium channels, and also to the inhibition of intracellular Ca(2+) release. The vasorelaxation was at partly related to the increase of prostacyclin (PGI(2)) induced by SO(2) derivatives.