Aim In order to study the change and role of apoptosis in hypertensive left ventricular remodeling. Methods Hearts from 16-week-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY) were investigated. Apoptosis in left ventricle sections was assessed by an in situ end-labeling technique (TUNEL), the feature and type of cells undergoing apoptosis were identified ultrastructurally by transmission electron microscope (ECM). Additionally, localization of Fas protein- a mediator of apoptotic cell death was examined by immunohistochemistry. Results Compared with 16-week-old WKY, 16-week-old SHR exhibited increased hypertrophic index, the apoptotic frequency of myocytes was also increased(19.54±7.27 vs 6.92±4.35/104 nucleus,P<0.05), whereas the apoptotic frequency of fibroblasts was significantly decreased (5.88±2.15 vs 14.34±9.56/104 nucleus,P<0.05). Moreover, apoptotic endothelial cells and leukocytes infiltrated into myocardium were also identified in SHR. Features of apoptotic myocytes and endothelial cells were observed by ECM in SHR. The latter often occurred in shrunken capillaries surrounded by collagen fragments The distribution of Fas antigen protein was mainly confined to myocytes in SHR, but limited to interstitial fibroblasts in WKY, consistently with the type of cells undergoing apoptosis in these two strains. Conclusion This study first suggest that apoptosis of different cell type may work synthetically in hypertensive myocardial remodeling, and Fas antigen may be associated with the mechanisms of these apoptotic process. Our findings also have important significance in searching new avenues for treatment with appropriate site-specific physiological or pharmacological regulators of apoptosis.