Koh Kwang Kon, Han Seung Hwan, Ahn Jeong Yeal, Chung Wook-Jin, Lee Yonghee, Shin Eak Kyun
Gil Medical Center, Gachon University, Incheon, Korea.
Int J Cardiol. 2009 Mar 20;133(1):23-31. doi: 10.1016/j.ijcard.2007.11.058. Epub 2008 Jan 15.
Reciprocal relationships between endothelial dysfunction and insulin resistance imply that improvement in endothelial dysfunction will have beneficial metabolic consequences. We hypothesized that amlodipine therapy in hypertensive subjects will improve endothelial dysfunction and metabolic parameters.
Amlodipine (10 mg daily for 8 weeks) or placebo was given to each 45 patients with mild to moderate hypertension in a randomized, double-blind, placebo-controlled, and parallel study. Age, sex, and body mass index were matched.
Amlodipine therapy significantly reduced systolic and diastolic blood pressure and increased HDL-cholesterol to greater extent than placebo therapy (all P<0.001). Amlodipine therapy significantly improved flow-mediated dilator response to hyperemia and reduced plasma malondialdehyde levels to a greater extent than placebo (P<0.001 and P=0.035). Amlodipine therapy significantly increased plasma adiponectin levels (P=0.009) and decreased plasma leptin and resistin levels (P<0.001 and P=0.025, respectively) to a greater extent than placebo. Correlations were noted between percent changes in adiponectin levels and percent changes in HDL-cholesterol (r=0.348, P=0.019) and QUICKI (r=0.326, P=0.029) following amlodipine therapy. Only changes in HDL-cholesterol (beta=0.469, P=0.019) and QUICKI (beta=1.786, P=0.069) were independent predictors of changes in adiponectin levels (multivariate regression analysis). We also observed inverse correlations between percent changes in leptin levels and percent changes in QUICKI (r=-0.569, P<0.001) following amlodipine therapy with changes in QUICKI (beta=1.810, P<0.001) as an independent predictor of changes in leptin levels.
Amlodipine therapy improves blood pressure, endothelial function, and metabolic parameters in patients with hypertension.
内皮功能障碍与胰岛素抵抗之间的相互关系表明,改善内皮功能障碍将产生有益的代谢后果。我们假设氨氯地平治疗高血压患者将改善内皮功能障碍和代谢参数。
在一项随机、双盲、安慰剂对照的平行研究中,对45例轻度至中度高血压患者分别给予氨氯地平(每日10mg,共8周)或安慰剂。年龄、性别和体重指数相匹配。
与安慰剂治疗相比,氨氯地平治疗显著降低收缩压和舒张压,并使高密度脂蛋白胆固醇升高幅度更大(均P<0.001)。与安慰剂相比,氨氯地平治疗显著改善了血流介导的充血扩张反应,并使血浆丙二醛水平降低幅度更大(P<0.001和P=0.035)。与安慰剂相比,氨氯地平治疗使血浆脂联素水平显著升高(P=0.009),并使血浆瘦素和抵抗素水平降低幅度更大(分别为P<0.001和P=0.025)。氨氯地平治疗后,脂联素水平变化百分比与高密度脂蛋白胆固醇变化百分比(r=0.348,P=0.019)以及定量胰岛素敏感性检查指数(QUICKI)(r=0.326,P=0.029)之间存在相关性。在多因素回归分析中,只有高密度脂蛋白胆固醇变化(β=0.469,P=0.019)和QUICKI变化(β=1.786,P=0.069)是脂联素水平变化的独立预测因素。氨氯地平治疗后,我们还观察到瘦素水平变化百分比与QUICKI变化百分比之间呈负相关(r=-0.569,P<0.001),其中QUICKI变化(β=1.810,P<0.001)是瘦素水平变化的独立预测因素。
氨氯地平治疗可改善高血压患者的血压、内皮功能和代谢参数。