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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Reduction of asymmetric dimethylarginine involved in the cardioprotective effect of losartan in spontaneously hypertensive rats.
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Reduction of asymmetric dimethylarginine involved in the cardioprotective effect of losartan in spontaneously hypertensive rats.

机译：氯沙坦对自发性高血压大鼠心脏保护作用的不对称二甲基精氨酸的减少。

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Previous studies have indicated that nitric oxide synthase (NOS) inhibitors can induce an increase of blood pressure and exacerbate myocardial injury induced by ischemia and reperfusion, whereas angiotensin II receptor antagonists protect the myocardium against injury induced by ischemia and reperfusion. Isolated hearts from male spontaneously hypertensive rats (SHR) or male Wistar-Kyoto rats (WKY) were subjected to 20 min global ischemia and 30 min reperfusion. Heart rate, coronary flow, left ventricular pressure, and its first derivatives (+/-dP/dt(max)) were recorded, and serum concentrations of asymmetric dimethylarginine (ADMA) and NO and the release of creatine kinase in coronary effluent were measured. The level of ADMA was significantly increased and the concentration of NO was decreased in SHR. Ischemia and reperfusion significantly inhibited the recovery of cardiac function and increased the release of creatine kinase, and ischemia and reperfusion-induced myocardial injury in SHR was aggravated compared with WKY. Vasodilation responses to acetylcholine of aortic rings were decreased in SHR. Treatment with losartan (30 mg/kg) for 14 days significantly lowered blood pressure, elevated the plasma level of NO, and decreased the plasma concentration of ADMA in SHR. Treatment with losartan significantly improved endothelium-dependent relaxation and cardiac function during ischemia and reperfusion in SHR. Exogenous ADMA also aggravated myocardial injury induced by ischemia and reperfusion in isolated perfused heart of WKY, as shown by increasing creatine kinase release and decreasing cardiac function. The present results suggest that the protective effect of losartan on myocardial injury induced by ischemia and reperfusion is related to the reduction of ADMA levels.
机译：先前的研究表明，一氧化氮合酶（NOS）抑制剂可引起血压升高，并加剧缺血和再灌注引起的心肌损伤，而血管紧张素II受体拮抗剂可保护心肌免受缺血和再灌注引起的损伤。对雄性自发性高血压大鼠（SHR）或雄性Wistar-Kyoto大鼠（WKY）的离体心脏进行20分钟的整体缺血和30分钟的再灌注。记录心率，冠状动脉血流，左心室压力及其一阶导数（+/- dP / dt（max）），并测量冠状流出物中的不对称二甲基精氨酸（ADMA）和NO的血清浓度以及肌酸激酶的释放。 SHR中ADMA的水平显着增加，NO的浓度降低。与WKY相比，缺血和再灌注显着抑制心脏功能的恢复，并增加肌酸激酶的释放，并且缺血和再灌注引起的心肌损伤加重。 SHR降低了对主动脉环乙酰胆碱的血管舒张反应。氯沙坦（30 mg / kg）治疗14天可显着降低血压，升高NO血浆水平，并降低SHR中ADMA的血浆浓度。氯沙坦治疗可显着改善SHR缺血和再灌注期间的内皮依赖性舒张功能和心脏功能。外源性ADMA还加重了孤立的WKY灌注心脏缺血和再灌注引起的心肌损伤，如肌酸激酶释放增加和心脏功能下降所显示。目前的结果表明，氯沙坦对缺血和再灌注引起的心肌损伤的保护作用与降低ADMA水平有关。

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