Sulfur dioxide derivatives improve the vasorelaxation in the spontaneously hypertensive rat by enhancing the vasorelaxant response to nitric oxide
Sulfur dioxide derivatives improve the vasorelaxation in the spontaneously hypertensive rat by enhancing the vasorelaxant response to nitric oxide
复制标题
二氧化硫衍生物通过增强对一氧化氮的血管舒张反应来改善自发性高血压大鼠的血管舒张作用
DOI：
10.1258/ebm.2012.011304
复制
发表时间：
2012-07-01
影响因子：
3.2
通讯作者：
Jin, Hongfang
中科院分区：
文献类型：
--
作者：
Lu, Wei;Sun, Yan;Jin, Hongfang
本研究旨在探讨二氧化硫（SO2）对自发性高血压大鼠（SHR）血管舒张的调节作用。22只Wistar大鼠和15只SHR随机分为WKY对照组（n = 8）、WKY+ Na_2SO_3/NaHSO_3组（n = 8）、WKY+ HDX组（n = 6）、SHR对照组（n = 8）和SHR+ Na_2SO_3/NaHSO_3组（n = 7）。用尾部容积描记法测量大鼠在体血压。实验中分别测定了乙酰胆碱（Ach）和硝普钠（SNP）对大鼠胸主动脉的舒张反应。同时，测定HDX孵育后WKY主动脉SO2含量和HDX孵育后血管对Ach的舒张反应。测定各组大鼠主动脉一氧化氮（NO）生成量。用NO抑制剂N-硝基-L-精氨酸甲酯（L-NAME）孵育WKY大鼠主动脉，测定其对不同浓度SO_2的舒张反应。SO2衍生物能显著降低SHR的血压（P < 0.05）。内源性SO_2的减少可使Ach引起的血管舒张作用减弱。与SHR对照组相比，SO2衍生物处理的SHR血管对Ach和SNP的舒张反应增强，而HDX处理的WKY血管对Ach和SNP的舒张反应减弱（P < 0.05）。SO_2衍生物组动脉组织NO水平升高（P < 0.05）。然而，与WKY对照组相比，在l-NAME存在下对SO2衍生物的血管舒张反应显著降低。结果提示，SO2通过增强NO对SHR离体主动脉环的舒张反应，增加主动脉组织中NO的含量，降低血压，增强血管舒张作用。
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.