Anti-inflammatory and metabolic effects of candesartan in hypertensive patients

BackgroundAngiotensin II type 1 (AT1) receptor blocker therapy prevented or retarded 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.MethodsWe administered placebo or candesartan 16 mg daily during 2 months to 45 patients with mild to moderate hypertension. This study was randomized, double-blind, placebo-controlled, crossover in design.ResultsCandesartan therapy significantly lowered both systolic and diastolic blood pressure. 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 soluble CD40 ligand levels by 30 ± 11% (P < 0.001). There were significant inverse correlations between body mass index and baseline plasma adiponectin levels (r = − 0.480, P = 0.009). There were significant correlations between baseline adiponectin levels and baseline insulin (r = − 0.317, P = 0.034) or baseline Quantitative Insulin-Sensitivity Check Index (QUICKI), a surrogate index of insulin sensitivity (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 15 ± 4% (P = 0.012) and increased QUICKI by 8 ± 2% (P = 0.007). There were significant correlations between percent changes in adiponectin levels and percent changes in insulin (r = − 0.340, P = 0.022) or QUICKI (r = 0.325, P = 0.029).ConclusionsCandesartan therapy significantly reduced inflammation and increased adiponectin levels and improved insulin sensitivity in hypertensive patients.