The vasodilator mechanism of sulfur dioxide on isolated aortic rings of rats: Involvement of the K+ and Ca2+ channels.

The present study was designed to investigate vasodilator effect of endogenous gaseous sulfur dioxide (SO(2)) and roles of Ca(2+) channels and K(+) channels in relaxations of SO(2) in isolated rat aortic rings. Isolated rat aortic rings were perfused in organ baths and changes in isometric tension were recorded. The results showed that: (1) SO(2) could relax isolated aortic rings contracted by norepinephrine in a dose-dependent manner (EC(50), 1247.38+/-98.32 microM). The vasorelaxant effect of SO(2) at basal (110.34+/-35.22 microM) and low concentrations (<450 microM) was endothelium-dependent, while it was endothelium-independent at high concentrations (>500 microM). (2) The vasorelaxation of 1500 microM SO(2) on both endothelium-intact and endothelium-denuded aortic rings was partially inhibited by nifedipine, an L-type calcium-channel blocker. (3) The vasoconstriction responses induced by CaCl(2) were inhibited by 1500 microM SO(2) on both endothelium-intact and endothelium-denuded aortic rings. (4) The initial fast vasoconstriction induced by intracellular Ca(2+) release was enhanced by 1500 microM SO(2), but the sustained vasoconstriction evoked by extracellular Ca(2+) influx was inhibited by 1500 microM SO(2). (5) Pretreated by 1500 microM SO(2), the vasoconstriction responses induced by norepinephrine or KCl were enhanced at low concentrations and inhibited at high concentrations. (6) The SO(2)-induced vasorelaxation was partially inhibited by tetraethylammonium (TEA) and glibenclamide for both endothelium-intact and endothelium-denuded rings. For the endothelium-intact rings, the vasorelaxant effects induced by 30 and 300 microM SO(2) were partially inhibited by iberiotoxin. These results led to the conclusions that endogenous gaseous SO(2) could cause vasorelaxation on rat aortic rings in a dose-dependent manner. The vasorelaxant effects of SO(2) at basal and low concentrations were endothelium-dependent, which might be partly related to big-conductance Ca(2+)-activated K(+)(BK(Ca)) channel. The mechanism of SO(2)-induced vasorelaxation at high concentrations was shown to be endothelium-independent, which might be related to ATP-sensitive K(+)(K(ATP)) channel and L-type calcium-channel as well as possible alterations in Ca-influx and release pathways.