Downregulation angiotensin Ⅱ type 1 receptors expression and depletion ROS by hydrogen sulfide defend myocardial damage in renal vascular hypertension rats

【作者】 武宇明； 刘尚雨； 肖琳； 薛红梅； 郭琪；

【机构】 河北医科大学生理研究室；

【摘要】 Hydrogen sulfide(H2S)plays an important role in cardiovascular system.The major mechanism of renal vascular hypertension consists of over-activation of renin-angiotensin system(RAS).In addition,the function of angiotensin Ⅱ(Ang Ⅱ)via angiotensin Ⅱ type 1(AT1)receptors is a leading cause for blood pressure increasing and cardiac injury.Therefore,our experiment investigated the effect of H2S on AT1receptors expression and cardiac injury.After successfully copied a renal vascular hypertension model via2K1C(2 kidney 1 clip)operation,rats were applied a H2S donor Na HS(56μmol/Kg per d,intraperitoneally)for 4 weeks in order to investigate the protection of H2S exert on cardiac injury.The results proved that H2S protect against injury in cardiac function through reducing blood pressure,downregulating plasma Ang Ⅱ level and AT1 receptors expression in 2K1C rats.As for in vitro Ang Ⅱ induced cardiomyocytes injury,H2S analogically downregulate AT1 receptors expression in cardiomyocytes,which possibly results from depletion of ROS and upregulation of SOD-1.更多还原

【Abstract】 Hydrogen sulfide(H2S) plays an important role in cardiovascular system.The major mechanism of renal vascular hypertension consists of over-activation of renin-angiotensin system(RAS).In addition,the function of angiotensin Ⅱ(Ang Ⅱ) via angiotensin Ⅱ type 1(AT1) receptors is a leading cause for blood pressure increasing and cardiac injury.Therefore,our experiment investigated the effect of H2 S on AT1 receptors expression and cardiac injury.After successfully copied a renal vascular hypertension model via 2K1C(2 kidney 1 clip) operation,rats were applied a H2 S donor Na HS(56μmol/Kg per d,intraperitoneally) for 4 weeks in order to investigate the protection of H2 S exert on cardiac injury.The results proved that H2 S protect against injury in cardiac function through reducing blood pressure,downregulating plasma Ang Ⅱ level and AT1 receptors expression in 2K1 C rats.As for in vitro Ang Ⅱ induced cardiomyocytes injury,H2 S analogically downregulate AT1 receptors expression in cardiomyocytes,which possibly results from depletion of ROS and upregulation of SOD-1.更多还原