硫化氢对自发性高血压大鼠胸主动脉舒张反应的影响  

The influence of hydrogen sulfide on the relaxation activity of aorta in spontaneous hypertension rats

作　　者：闫辉[1] 杜军保[1] 唐朝枢[2] 

机构地区：[1]北京大学第一医院儿科,北京100034 [2]北京大学第一医院心血管病研究所,北京100034

出　　处：《中国药理学通报》2003年第6期633-636,共4页Chinese Pharmacological Bulletin

基　　金："985"重大心血管疾病基础研究基金;国家"973"重点基础研究发展规划项目资助课题;NO G2000056905

摘　　要：目的 探讨内源性及外源性硫化氢(H_2S)对自发性高血压大鼠(SHR)离体胸主动脉舒张反应的影响。方法 4wb WKY大鼠24只,随机分为WKY对照组(n=8)、WKY+H_2S组(n=8)及WKY+PPG组(n=8)。同样周龄SHR大鼠24只,随机分为高血压对照组(n=8)、高血压+H_2S组(n=8)及高血压+PPG组(n=8),高血压对照组及WKY对照组大鼠每日腹腔注射生理盐水,WKY+H_2S组及高血压+H_2S组每日腹腔注射硫氢化钠(NaHS),WKY+PPG组及高血压+PPG组每日腹腔注射PPG,5 wk后处死,取胸主动脉,观察其对乙酰胆碱(ACh)、硝普钠(SNP)及NaHS的舒张反应。结果 WKY+PPG组及高血压对照组、高血压+PPG组对ACh及SNP的舒张率较WKY组降低(P<0.05),而高血压+H_2S组较高血压对照组升高(P<0.05),与WKY对照组相似;各组大鼠血管环对SNP的舒 张反应均高于ACh(P<0.05);WKY对照组及高血压对照组对不同浓度的NaHS呈现剂量依赖性舒张反应,对于同样浓度的NaHS,高血压对照组较WKY对照组的舒张率高。结论 H_2S可以独立及与一氧化氮协同发挥舒张血管效应,在自发性高血压血管舒张功能异常的形成机制中占据重要地位。AIM To explore the influences of both endogenous and exogenous hydrogen sulfide on the relaxation reaction of aorta in spontaneous hypertension rats. METHODS Twenty-four male hypertension rats and WKY rats of 4 weeks old were randomly divided into control group, hydrogen sulfide group and PPG group, respectively. The blood pressure and the reactivity of aorta rings in response to acetylcholine, nitroprusside and different doses of hydrogen sulfide were measured five weeks later. RESULTS The relaxation activity to acetylcholine and nitroprusside in SHR+con-trol, SHR+PPG and WKY + PPG groups de- creased compared with that of WKY control rats (P<0. 05). The relaxation activity in SHR+hy-drogen sulfide was higher than that of SHR control group(P<0. 05). The relaxation activities in both SHR control group and WKY control group showed dose reliance increase in response to different doses of hydrogen sulfide. CONCLUSION Hydrogen sulfide worked as a vasorelaxator either independently or accompanied with nitric oxide, which played an important role in the development of spontaneous hypertension.

关 键 词：自发性高血压 胸主动脉 硫化氢 

分 类 号：R-332[医药卫生] R322.121