Effects of sodium hydrosulfide on cardiac function and activity of renin-angiotensin-aldosterone system in rats with chronic heart failure / 中国病理生理杂志

ABSTRACT

AIM:To investigate the effect of sodium hydrosulfide(NaHS)on cardiac function and activity of renin-angiotensin(Ang)-aldosterone(ALD)system(RAAS)in the rats with chronic heart failure(CHF).METHODS:The CHF rat model was established by abdominal aortic coarctation.SD rats were randomly divided into sham operation group,model group,low dose of NaHS group and high dose of NaHS group(n=6).The left ventricular end-diastolic di-ameter(LVEDD), left ventricular end-systolic diameter(LVESD)and left ventricular ejection fraction(LVEF)were measured before and after treatment by echocardiography in each group.The levels of renin,AngⅡand ALD in the plasma were measured by ELISA.The expression of angiotensin-converting enzyme(ACE)and angiotensin Ⅱ type 1 receptor (AT1R)at mRNA and protein levels in the myocardium tissues was determined by qPCR and Western blot,respectively. RESULTS:After treatment with NaHS,compared with model group and before treatment,LVEDD and LVESD in low dose of NaHS group and high dose of NaHS group were decreased significantly, while LVEF was increased significantly(P<0.05).Compared with low dose of NaHS group,LVEDD and LVESD were decreased,while LVEF was increased in high dose of NaHS group(P<0.05).Compared with sham operation group,the levels of renin,AngⅡand ALD in the plasma of model group were significantly increased(P<0.05),and the expression of ACE and AT1R at mRNA and protein levels in the myocardium tissues of model group were significantly increased(P<0.05).Compared with model group,the plas-ma levels of renin,AngⅡand ALD in low dose of NaHS group and high dose of NaHS group were significantly decreased (P<0.05),and the myocardial expression of ACE and AT 1R at mRNA and protein levels was significantly down-regulated (P<0.05).The plasma levels of renin,AngⅡand ALD,and the myocardial expression of ACE and AT 1R at mRNA and protein levels in high dose of NaHS group were significantly lower than those in low dose of NaHS group(P<0.05). CONCLUSION:NaHS inhibits the activation of RAAS,thus improving the cardiac function of CHF rats,and the effect of high-dose NaHS is better than that of low-dose NaHS.