Figure 4

Atherosclerotic lesion formation. Diabetic and non-diabetic ApoE^−/−-mice were treated 18 weeks with telmisartan, GW9662, telmisartan and GW9662 or vehicle, whereas diabetic and non-diabetic ApoE^−/−/AT1R^−/−-mice treated with GW9662 or vehicle. Representative histological cross-sections of the aortic root were stained with oil red O to analyse atherosclerotic plaque development, Figure 4A-F (diabetic animals) and Figure 4H-M (non-diabetic animals). Quantitative analysis of atherosclerotic lesion formation indicated as plaque area in % of total area is depicted in Figure 4G (diabetic animals) and Figure 4N (non-diabetic animals). Diabetic ApoE^−/−-mice displayed increased atherosclerotic lesion formation. AT1R-deficiency and telmisartan treatment in ApoE^−/−-mice resulted in a significantly reduced area of atherosclerotic lesions, whereas GW9662 antagonized the atheroprotective effects of AT1R deficiency or AT1 antagonism. ^*P < 0.05 vs. diabetic and non-diabetic ApoE^−/−, ^#P < 0.05 vs. diabetic ApoE^−/−/AT1R^−/−, ^‡P < 0.05 vs diabetic and non diabetic ApoE^−/− + GW9662, n = 6-8 per group.