Sulfur dioxide relaxes rat aorta by endothelium-dependent and -independent mechanisms

This study aimed to investigate the vasoactivity of sulfur dioxide(SO2), a novel gas identified from vascular tissue, in rat thoracicaorta. The thoracic aorta was isolated, cut into rings, andmounted in organ-bath chambers. After equilibrium, the ringswere gradually stretched to a resting tension. Isometric tensionwas recorded under the treatments with vasoconstrictors, SO2derivatives, and various drugs as pharmacological interventions.In endothelium-intact aortic rings constricted by 1 μMphenylephrine (PE), SO2 derivatives (0.5 – 8 mM) caused a dosedependent relaxation. Endothelium removal and a NOS inhibitorL-NAME reduced the relaxation to low doses of SO2 derivatives,but not that to relatively high doses (≥ 2 mM). In endotheliumdenuded rings, SO2 derivatives attenuated vasoconstrictioninduced by high K+ (60 mM) or CaCl2 (0.01-10 mM). Therelaxation to SO2 derivatives in PE-constricted rings withoutendothelium was significantly inhibited by blockers of ATPsensitive K+ (KATP) and Ca2+-activated K+ (KCa) channels, but notby those of voltage-dependent K+ channels, Na+-K+-ATPase orNa+-Ca2+ exchanger. SO2 relaxed vessel tone via endotheliumdependent mechanisms associated with NOS activation, and viaendothelium-independent mechanisms dependent on theinhibition of voltage-gated Ca2+ channels, and the opening of KATPand KCa channels.