Abstract: AIM:To investigate the role of Src in the pathogenesis of left ventricular hypertrophy resulting from pressure load. METHODS: Expressions and subcellular location of Src were determined using immunofluorescent labeling, confocal microscopy and Western blotting in cardiac myocytes of hypertrophic left ventricle from 2-, 6-, 12-, and 18-month-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) control rats. RESULTS: No significant difference was seen in Src expression in the left ventricle tissue homogenate including total protein among 2-, 6-, 12- and 18-month-old SHR and age-matched WKY rats, and no significant difference was observed in the cytoplasmic fraction and membrane fraction between 2-month-old SHR and WKY rats. The expression of Src significantly decreased in cytoplasmic fraction from 6-, 12- and 18-month-old SHR, whereas expression of Src significantly increased in the membrane fraction from 6-, 12- and 18-month-old SHR as compared with those in age-matched WKY rats. Confocal microscopy confirmed that as more Src accumulated, more wide fluorescent bands were observed in the intercalated disks of cardiac myocytes from 6-, 12- and 18-month-old SHR compared with what was observed in age-matched WKY control rats. CONCLUSIONS: Subcellular redistribution of Src in the hypertrophic left ventricle of SHR indicates that Src kinase signal transduction pathway may play a critical role in myocardial remodeling in decompensated hypertensive ventricular hypertrophy.