Abstract: AIM:To explore the metabolic characteristics of type I collagen in rats with pressure-overloaded left ventricular hypertrophy and the effect of telmisartan intervention. METHODS: Twenty-four male Spargue Dawley rats were randomly divided into three groups: sham-operation group (n=8), left ventricular hypertrophy group (n=8) and telmisartan group (n=8). Abdominal aorta constriction operation was performed to construct a rat model of hypertensive left ventricular hypertrophy. Rats in each group were killed after 4 weeks of treatment. Body and left ventricular mass were weighed and left ventricular mass index (LVMI) was calculated. Left cardiac ventricle was stained with Masson and observed. The collagen volume fraction (CVF) was measured. ELISA was employed to detect serum carboxy-terminal propeptide of type I procollagen (PICP) and type I collagen carboxy-terminal cross-linked peptide (ICTP) concentration to calculate the ratio of PICP to ICTP in the three groups. Linear correlation analysis was conducted to analyze, respectively, the correlation between PICP and CVF and between the ratio of PICP to ICTP and CVF. RESULTS: Compared with those in sham-operation group, left ventricular mass, LVMI, CVF, serum PICP and the ratio of PICP to ICTP in left ventricular hypertrophy group all significantly increased (all P<0.05) and compared with those in left ventricular hypertrophy group, left ventricular mass, LVMI, CVF, serum PICP and the ratio of PICP to ICTP in the telmisartan group all significantly decreased (all P<0.05). No statistical difference was observed in ICTP among the three groups. Both PICP and the ratio of PICP to ICTP were positively related with CVF (all P<0.01). CONCLUSION: Type I collagen synthesis in rats with pressure-overloaded left ventricular hypertrophy increases and its degradation is relatively insufficient and the imbalance between synthesis and degradation is one cause of cardiac mesenchymal fibrosis. Telmisartan could inhibit the synthesis of type I collagen and improve the balance between its synthesis and degradation, which effectively inhibits and reverses the cardiac mesenchymal fibrosis.