Aim To investigate the effect of telmisartan on rabbit apoptotic cardiomyocytes underwent ischemia/reperfusion(I/R) injury. Methods 48 Healthy male New Zealand white rabbits were randomly divided into six groups(n=8): sham operation group,I/R model group,GW9662 group,telmisartan group,telmisartan+GW9662 group,candesartan group.After intragastric administration for 2 weeks,the left anterior descending(LAD) coronary artery was occluded for 60 minutes followed by 360 minutes reperfusion to induce ischemia/reperfuion injury.The concentration of angiotensinⅡ in myocardium was analyzed by radioimmunoassay and the intracellular free calcium concentration was measured by dual wavelength fluorophotometry.Then,protein expression of peroxisome proliferator activated receptor-γ(PPARγ) was detected by Western blot.In addition,apoptosis was detected by transmission electron microscope and by TUNEL staining. Results Compared with sham operation group,the concentration of angiotensinⅡin myocardium was significantly increased in I/R model group,GW9662 group,telmisartan group,telmisartan+GW9662 group,and candesartan group(P<0.01).And,the expression of PPARγ was higher in telmisartan group than that in other groups(P<0.01).Interestingly,telmisartan,telmisartan+GW9662 and candesartan inhibited the morphological chan ges of apoptotic cardiomyocytes,which was induced by myocardial ischemia/reperfusion,by condensing chromatin clumps against the nuclear envelope and presentation of apoptotic body.When compared with I/R model group,the intracellular free calcium concentration and apoptosis index were significantly reduced in telmisartan group,telmisartan+GW9662 group and candesartan group(P<0.01).Among them,apoptosis index was lowest in telmisartan group(P<0.01). Conclusion Telmisartan could reduce myocardial apoptosis by blocking the angiotensinⅡreceptor and up-regulating the expression of PPARγ in the rabbit I/R model.