Figure 2

Vascular function. After 18 weeks aortic segments of diabetic (A) and non-diabetic (B) ApoE^−/− and ApoE^−/−/AT1R^−/−-mice were isolated and their functional performance was assessed in organ chamber experiments. Endothelium-dependent vasodilation induced by carbachol is shown. Diabetic ApoE^−/−-mice displayed severe impairment of endothelial function compared to ApoE^−/−/AT1R^−/−-mice and telmisartan-treated ApoE^−/−-mice. Treatment of diabetic ApoE^−/− and ApoE^−/−/AT1R^−/−-mice with GW9662 antagonized the protective vascular effects of AT1R deficiency or AT1 antagonism. ^*P < 0.05 vs. diabetic ApoE^−/−, ^#P < 0.05 vs. diabetic ApoE^−/−/AT1R^−/− and ^‡P < 0.05 vs diabetic ApoE^−/− + Telmisartan + GW9662, n = 6-8 per group.