Background: Angiotensin II type 1 (AT1) receptor blocker therapy prevented the progression of coronary heart disease. The mechanisms of this benefit may relate to the ability of AT1 receptor blockers to reduce inflammation and insulin resistance. Methods: We administered placebo or candesartan 16 mg daily during 2 months to 45 patients with hypertension. This study was randomized, double-blind, placebo-controlled, crossover in design. Results: Candasartan therapy significantly lowered blood pressure and improved flow-mediated dilation and decreased plasma malondialdehyde levels. Compared with placebo, candesartan therapy significantly lowered plasma hsCRP levels relative to baseline measurements from 1.10 to 0.70 mg/l (P=0.024) and sCD40L levels by 30짹11% (P<0.001) and TNF-慣 by 10짹4% (P=0.026) and MCP-1 by 9짹3% (P=0.003). There were significant correlations between baseline adiponectin levels and baseline HDL-cholesterol levels (r=0.499, p<0.001), insulin (r=-0.317, p=0.034), or baseline QUICKI (r=0.371, p=0.012). Compared with placebo, candesartan therapy significantly lowered fasting insulin levels (P=0.011) and increased plasma levels of adiponectin by 15짹4% (P=0.012) and increased QUICKI by 8짹2% (P=0.007). There were significant correlations between percent changes in adiponectin levels and percent changes in HDL-cholesterol (r=0.309, p=0.041), insulin (r=-0.340, p=0.022), or QUICKI (r=0.325, p=0.029). Conclusions: Candesartan therapy significantly improved the percent flow-mediated dilator response to hyperemia and reduced levels of oxidant stress and inflammation markers and increased adiponectin levels and improved insulin sensitivity in hypertensive patients.