Sulfur dioxide upregulates the aortic nitric oxide pathway in rats

Sulfur dioxide (SO(2)) is a common gaseous pollutant. It is also, however, endogenously generated from sulfur-containing amino acids. Recent studies have demonstrated that rat blood pressure can be lowered by SO(2)-exposure in vivo and that vasodilation caused by SO(2) at low concentrations (<450 microM) is endothelium-dependent in rat aorta. However, effects of SO(2) on nitric oxide synthase (NOS) and nitric oxide (NO) production have not been previously studied in rat aorta. The objective of the present study is to assess the effects of acute (10 min) and prolonged (2h) stimulation with different concentrations of SO(2) on NO/cGMP pathway in isolated rat aorta. The results show that: (1) the acute and prolonged pretreatments with SO(2) produced an inhibition of vasoconstrictions induced by norepinephrine. (2) SO(2) potentiated activity of endothelial nitric oxide synthase (eNOS), but not of induced NOS (iNOS). (3) SO(2) could increase expression of eNOS gene on the transcription and translation levels in rat aorta. (4) SO(2) enhanced NO formation in aortic tissue. (5) The level of cGMP in rat aorta was increased by SO(2) and no change of cAMP. These findings led to the conclusion: there were acute and prolonged effects of SO(2) on the NO/cGMP signalling pathway; and SO(2) could upregulate the eNOS-NO-cGMP pathway and at least partly by which the SO(2) might cause vasodilation and inhibition to vasoconstriction.