Hypertensive　myocardial　remodeling　has　an　important　role　in　the　pathophysiology　of　hypertensive　disease.　This　study　suggests　that　telmisartan　(TEL)　can　inhibit　myocardial　fibrosis　of　hypertensive　left　ventricular　hypertrophy　(LVH)　through　the　transforming　growth　factor-beta　1　(TGF-beta　1)/Smad　signaling　pathway.　Through　echocardiography　and　hemodynamics,　it　was　shown　that　TEL　could　improve　cardiac　function　and　reduce　the　degree　of　hypertensive　LVH　in　hypertensive　rats.　Through　immunoassay,　it　was　shown　that　TEL　could　antagonize　renin-angiotensin-aldosterone　system　expression　in　plasma　and　myocardial　tissue.　By　Masson　staining,　Elisa　and　alkaline　hydrolysis　assays,　it　was　demonstrated　that　TEL　could　significantly　inhibit　myocardial　fibrosis　in　hypertensive　rats　and　attenuate　extracellular　matrix-related　proteins　associated　with　pressure　overload.　Western　blotting　was　used　to　detect　the　TGF-beta　1/Smad　signaling　pathway　protein　expression　of　myocardial　tissue,　and　it　was　further　found　that　TEL　could　inhibit　activation　of　the　TGF-beta　1/Smad　signaling　pathway.　In　conclusion,　TEL　could　inhibit　myocardial　local　angiotensin　II　(Ang　II)　level　by　directly　affecting　the　Ang　II　receptor.　TEL　may　also　restore　the　balance　of　matrix　metalloproteinases/tissue　inhibitor　of　metalloproteinases,　reduce　myocardial　collagen　fibrosis　and　delay　hypertensive　LVH　by　affecting　the　TGF-beta　1/Smad　signaling　pathway.