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肥胖导致高血压的机制。

Mechanisms of obesity-induced hypertension.

机构信息

3rd Department of Medicine, Hypertension Center, Papageorgiou Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece.

出版信息

Hypertens Res. 2010 May;33(5):386-93. doi: 10.1038/hr.2010.9.

Abstract

The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies.

摘要

肥胖与高血压的关系在儿童和成人中都已得到充分证实。肥胖直接导致高血压的机制仍在研究中。交感神经系统的激活被认为在肥胖相关高血压的发病机制中具有重要作用。根据无限反馈增益的原则,利尿和利钠的动脉压控制机制似乎在肥胖个体中向更高的血压水平转移。在肥胖的早期阶段,由于肾小管重吸收增加,原发性钠潴留存在。细胞外液容量扩张,肾脏液装置重置为高血压水平,符合容量超负荷引起的高血压模型。肥胖期间,血浆肾素活性、血管紧张素原、血管紧张素 II 和醛固酮水平显著升高。胰岛素抵抗和炎症可能会导致血管功能改变,进而导致高血压。瘦素和其他神经肽可能是肥胖与高血压发展之间的联系。肥胖应被视为一种慢性疾病,可能需要长期治疗。了解与肥胖相关高血压相关的机制对于成功的治疗策略至关重要。

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