Abstract: Objective To investigate the effects of telmisartan on the protein profiles of left ventricular myocardial tissue in spontaneously hypertensive rats（SHR）. Methods Sixteen SHR were randomly divided into the control group and the telmisartan group. They were treated with sterile water for injection（10 mL/kg） or telmisartan（4.33 mg/kg） by intragastric administration. Wistar-Kyoto（WKY） rats treated with sterile water for injection（10 mL/kg） served as control. The treatment period was 12 weeks. After 12 weeks, those rats were sacrificed, and their heart samples were collected to make protein preparations. Subsequently, the separated part of the protein agent was subjected to isotope-labeled relative and absolute quantitative（iTRAQ） labeling and strong cation exchange column liquid phase separation and mass spectrometry identification using a tandem mass spectrometer. Finally, pathway-related proteins and their biochemical metabolic pathways and signal transduction pathways were selected via the differential protein pathway enrichment analysis. Results There were 23 differential proteins related to the pathway in total. Compared with the telmisartan group, the up-regulated differential proteins in the SHR group were prokinin kinase 3, transgelin, and haptoglobin subtype 2. The down-regulated differential proteins in the SHR group were as follows: von Willebrand factor（fragment）, kininogen 1, small ribonucleoprotein-related protein, fibrinogen beta chain, protein mass 3（fragment）, proteasome, heat shock protein 27-related protein 1, tenascin X, fibronectin subtype 2, transferrin receptor protein, platelets 1, cathepsin L1, complement factor B, isoform CRA_b, fibrinogen isomer, immunoglobulin heavy chain（γ polypeptide） and α₁ anti-protease. Conclusion Telmisartan may affect the left ventricular hypertrophy in hypertensive rats through heat shock protein 27, fibrinogen, fibronectin, proteasome 26 s and transgelin, as well as their biochemical metabolic pathways and signal transduction pathways.