Objective:To assess the effect of angiotensin II type 1(AT1)receptor antagonist losartan on myocardium con- nexin43(Cx43)gap junction(GJ)expression in spontaneously hypertensive rats(SHRs)and investigate possible mechanisms. Methods:Sixteen 9-week-old male SHRs and 8 age-matched male Wistar-Kyoto(WKY)rats were included in this study.SHRs were randomly divided into two groups to receive losartan at 30 mg/(kg·d)by oral gavage once daily for 8 weeks(SHR-L)or vehicle(0.9%saline)to act as controls(SHR-V);WKY rats receiving vehicle for 8 weeks served as normotensive controls.At the end of the experiment,rats were sacrificed and the hearts were removed.Expressions of Cx43 and nuclear factor-kappaB p65 (NF-κB p65)proteins in all three groups were observed and further investigations on the effect of angiotensin II type 1 receptor antagonist losartan(30 mg/(kg·d),8 weeks)on Cx43 expression were conducted with Western blot and immunohistochemistry. NF-κB p65 protein in nuclear extracts was determined by Western blot.Results:Left ventricular(LV)hypertrophy was prominent in SHRs,Cx43 and NF-κB p65 protein expressions were obviously upregulated and Cx43 distribution was dispersed over the cell surface.Treatment with losarton reduced the over-expressions of Cx43 and NF-κB p65 in LV myocardium.The distribution of Cx43 gap junction also became much regular and confined to intercalated disk after losartan treatment.Conclu- sion:Cx43 level was upregulated in LV myocardium of SHR during early stage of hypertrophy.Angiotensin II type 1 receptor antagonist losartan prevented Cx43 gap junction remodeling in hypertrophied left ventricles,possibly through the NF-κB pathway. Objective: To assess the effect of angiotensin II type 1 (AT1) receptor antagonist losartan on myocardium con- nexin43 (Cx43) gap junction (GJ) expression in spontaneously hypertensive rats (SHRs) and investigate possible mechanisms. Methods: Sixteen 9-week- old male SHRs and 8 age-matched male Wistar-Kyoto (WKY) rats were included in this study. SHRs were randomly divided into two groups to receive losartan at 30 mg / (kg.d) by oral gavage once daily for 8 weeks ( SHR-L) or vehicle (0.9% saline) to act as controls (SHR-V); WKY rats receiving vehicle for 8 weeks served as normotensive controls. At the end of the experiment, rats were sacrificed and the hearts were removed. Expressions of Cx43 and nuclear factor-kappaB p65 (NF-κB p65) proteins in all three groups were observed and further investigations on the effect of angiotensin II type 1 receptor antagonist losartan (30 mg / (kg · d), 8 weeks) on Cx43 expression were conducted with Western blot and immunohistochemistry. NF-κB p65 protein in nuclear extracts was de termined by Western blot. Results: Left ventricular (LV) hypertrophy was prominent in SHRs, Cx43 and NF-κB p65 protein expressions were obviously upregulated and Cx43 distribution was dispersed over the cell surface. Treatment with losarton reduced the over-expressions of Cx43 and NF-κB p65 in LV myocardium. The distribution of Cx43 gap junction also became much more regular and confined to intercalated disk after losartan treatment. Confluence: Cx43 level was upregulated in LV myocardium of SHR during early stage of hypertrophy. Angiotensin II type 1 receptor antagonist losartan prevented Cx43 gap junction remodeling in hypertrophied left ventricles, possibly through the NF-κB pathway.