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游泳运动后自发性高血压大鼠主动脉一氧化氮的变化及其对胱硫醚-γ-裂解酶/硫化氧体系的影响 被引量:2

Effects of swimming exercise on nitric oxide and CSE/H_2S in spontaneously hypertensive rats
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摘要 目的:观察运动对自发性高血压大鼠(SHR)主动脉一氧化氮合酶(NOS)、一氧化氮(NO)、胱硫醚-γ-裂解酶(CSE)和硫化氢(H_2S)的影响,探讨运动干预后SHR大鼠内源性NO的变化对主动脉CSE/H_2S体系的调节作用。方法:选用雄性SHR大鼠16只,随机分为高血压对照组(SC组)和高血压运动组(ST组),每组8只。同时选用雄性Wistar大鼠8只,为正常对照组(WC组)。ST组大鼠进行8周、每周6次、每次90min中等强度的无负重游泳运动。结果:8周90min游泳运动后,SC组大鼠血压较实验前显著升高(P<0.01),ST组大鼠血压较SC组大鼠血压显著下降(P<0.01),且与实验前相比无显著性差异(P>0.05);ST组大鼠较SC组大鼠主动脉NOS、NO、CSE和H_2S水平显著升高(P<0.05)。结论:运动可抑制SHR的血压上升,增加SHR主动脉NOS和NO的含量,内源性NO对SHR主动脉CSE/H_2S体系在运动缓解血压上升中呈促进作用,这一过程参与了运动降压的调控机制。 Objective: To study the effects of exercises on blood pressure and aorta nitric oxide synthase(NOS),nitric oxide (NO), cystathionine-7-1yase(CSE) and hydrogen sulfide in spontaneously hypertensive rats (SHR), then to ex- plore the regulation effects of exercise on endogenous NO and aorta CSE/H2S in SHR. Method: Sixteen male SHR were randomly divided into the SHR control group(SC) and SHR training group (ST); 8 rats in each group. Eight male Wistar rats were the normal matched control group(WC).ST group car- ries on 90 min moderate swimming, without load, 6 times a week. All rats feed normal feedstuff for 8 weeks. And then the rats' blood pressure(BP) were measured each week during experimental period, the contents of aorta NOS,NO, CSE and H:S were examined. Result: After 8-weeks swimming exercise, the BP in SHR training group was little higher than before, but no significant difference. However, in SHR control group it was just opposite (P〈0.01); the levels of aorta NOS, NO, CSE and H2S in SHR training group were significantly elevated(P〈0.05). Conclusion: Swimming exercise can inhibit the elevation of BP, increase the levels of aorta NOS and NO in SHR, and endogenous NO can promote the aorta CSE/H^S system in the process of exercise depressing the blood pressure elevation.
出处 《中国康复医学杂志》 CAS CSCD 北大核心 2013年第10期899-903,共5页 Chinese Journal of Rehabilitation Medicine
关键词 高血压 运动 一氧化氮 胱硫醚-Γ-裂解酶 硫化氢 hypertension exercise nitric oxide cystathionine-y-lyase H2S
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