Sulfur dioxide derivatives improve the vasorelaxation in the spontaneously hypertensive rat by enhancing the vasorelaxant response to nitric oxide.

The present study was designed to explore the role of sulfur dioxide (SO(2)) 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+Na(2)SO(3)/NaHSO(3) (n = 8), WKY+L-aspartic acid-β-hydroxamate (HDX) (n = 6), SHR control (n = 8) and SHR+Na(2)SO(3)/NaHSO(3) (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 SO(2) 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 SO(2) after incubation with the NO inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME). The blood pressure decreased significantly in SHRs treated with SO(2) derivatives (P < 0.05). Reduction of endogenous SO(2) 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 SO(2) 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 SO(2) derivatives (P < 0.05). However, the vasorelaxant response to SO(2) derivatives in the presence of L-NAME decreased markedly compared with WKY controls. The results suggest that SO(2) 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.