The present study was designed to explore the role of sulfur dioxide (SO2) in the regulation of vasorelaxation in the spontaneously hypertensive rat (SHR). Twenty-two Wistar rats and 15 SHRs were divided randomly into the following groups: Wistar-Kyoto (WKY) control (n = 8), WKY+Na2SO3/NaHSO3 (n = 8), WKY+l-aspartic acid-β-hydroxamate (HDX) (n = 6), SHR control (n = 8) and SHR+Na2SO3/NaHSO3 (n = 7). Their blood pressure in vivo was measured by tail plethysmography. The vasorelaxant response of the thoracic aorta to acetylcholine (Ach) and sodium nitroprusside (SNP) in all rats was tested, respectively, in the experiment. At the same time, the SO2 content of the WKY aorta after incubation with HDX and the vasorelaxant response to Ach after incubation with HDX were quantified. Nitric oxide (NO) production in the aorta of all rats was determined. We also measured the vasorelaxant responses of WKY aorta to different concentrations of SO2 after incubation with the NO inhibitor, N
G-nitro-l-arginine methyl ester (l-NAME). The blood pressure decreased significantly in SHRs treated with SO2 derivatives (P < 0.05). Reduction of endogenous SO2 in WKY vessels resulted in a decrease in the vasorelaxation induced by Ach. Vasorelaxation in response to both Ach and SNP increased in SHRs treated with SO2 derivatives compared with SHR controls, but decreased in WKY given HDX compared with WKY controls (P < 0.05). The NO level in arterial tissues increased in SHRs treated with SO2 derivatives (P < 0.05). However, the vasorelaxant response to SO2 derivatives in the presence of l-NAME decreased markedly compared with WKY controls. The results suggest that SO2 reduced blood pressure and increased vasorelaxation in SHR arteries via enhancing the vasorelaxant response to NO in isolated aortic rings and increasing the NO level of aortic tissues.
