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首页> 外文期刊>Circulation journal >Increased Tissue Angiotensin-Converting Enzyme Activity Impairs Bradykinin-Induced Dilation of Coronary Arterioles in Obesity
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Increased Tissue Angiotensin-Converting Enzyme Activity Impairs Bradykinin-Induced Dilation of Coronary Arterioles in Obesity

机译：组织中血管紧张素转换酶活性的增加损害了缓激肽诱导的肥胖患者冠状小动脉的扩张。

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Background: ?Bradykinin (BK) is a key mediator regulating coronary blood flow. It is degraded by angiotensin-converting enzyme (ACE), but what is unknown is whether enhanced tissue ACE activity interferes with BK-induced coronary vasodilation in obesity. Methods and Results: ?Coronary arterioles (～100μm) were isolated from rats on a normal or high-fat diet (HFD) and from lean or obese patients undergoing heart surgery (n=74). We found that BK-induced dilation was diminished in the coronary arterioles of HFD rats, when compared with controls. When administered in vitro, the ACE inhibitor, captopril, restored the coronary dilation response to BK in HFD rats, but did not affect control responses. Abundant ACE expression was detected in coronary endothelium, which was associated with increased ACE activity in HFD arterioles, as measured by increased response to the ACE substrate, angiotensin I. Moreover, we found that in the coronary arterioles of obese patients, BK-induced dilation was augmented by in vitro captopril administration. Correspondingly, ACE activity was increased in the coronary arterioles of obese patients when compared with the non-obese. Logistic regression analysis revealed that obese patients taking ACE inhibitors prior to surgery exhibited an enhanced dilation response to BK. Conclusions: ?We demonstrated augmented tissue ACE activity in the coronary arterioles of obese subjects, which leads to reduced coronary dilation response to BK. We provide a rationale for ACE inhibitor therapy in obese patients to improve dilatation of coronary microvessels.??(Circ J?2013; 77: 1867–1876)
机译：背景：缓激肽（BK）是调节冠状动脉血流量的关键介质。它会被血管紧张素转化酶（ACE）降解，但未知的是组织ACE活性增强是否会干扰肥胖症中BK诱导的冠状血管舒张。方法和结果：？从正常饮食或高脂饮食（HFD）的大鼠以及进行心脏手术的肥胖或肥胖患者（n = 74）中分离出冠状小动脉（〜100μm）。我们发现，与对照组相比，HFD大鼠的冠状小动脉中BK诱导的扩张减少。在体外给药时，ACE抑制剂卡托普利可恢复HFD大鼠对BK的冠状动脉扩张反应，但不影响对照反应。通过对ACE底物血管紧张素I的反应增强，可以在冠状动脉内皮中检测到大量ACE表达，这与HF活动小动脉中ACE活性增加有关。此外，我们发现，在肥胖患者的冠状动脉中，BK诱导的扩张通过体外卡托普利给药来增强。相应地，与非肥胖者相比，肥胖患者冠状动脉的ACE活性增加。 Logistic回归分析显示，在手术前服用ACE抑制剂的肥胖患者对BK的扩张反应增强。结论：？我们证明了肥胖受试者冠状动脉的组织ACE活性增强，这导致对BK的冠状动脉扩张反应降低。我们为肥胖患者提供ACE抑制剂治疗以改善冠状动脉微血管扩张的理论基础。（Circ J？2013; 77：1867-1876）

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