The Vasodilator Effect and Its Mechanism of Sulfur Dioxide-Derivatives on Isolated Aortic Rings of Rats

Abstract

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 (PGI₂) induced by SO₂ derivatives.