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瘦素在血压调节和动脉高血压中的作用。

Role of leptin in blood pressure regulation and arterial hypertension.

作者信息

Bełtowski Jerzy

机构信息

Department of Pathophysiology, Medical University, Lublin, Poland.

出版信息

J Hypertens. 2006 May;24(5):789-801. doi: 10.1097/01.hjh.0000222743.06584.66.

Abstract

Leptin is a 16-kDa protein secreted by white adipose tissue that is primarily involved in the regulation of food intake and energy expenditure. Plasma leptin concentration is proportional to the amount of adipose tissue and is markedly increased in obese individuals. Recent studies suggest that leptin is involved in cardiovascular complications of obesity, including arterial hypertension. Acutely administered leptin has no effect on blood pressure, probably because it concomitantly stimulates the sympathetic nervous system and counteracting depressor mechanisms such as natriuresis and nitric oxide (NO)-dependent vasorelaxation. By contrast, chronic hyperleptinemia increases blood pressure because these acute depressor effects are impaired and/or additional sympathetic nervous system-independent pressor effects appear, such as oxidative stress, NO deficiency, enhanced renal Na reabsorption and overproduction of endothelin. Although the cause-effect relationship between leptin and high blood pressure in humans has not been demonstrated directly, many clinical studies have shown elevated plasma leptin in patients with essential hypertension and a significant positive correlation between leptin and blood pressure independent of body adiposity both in normotensive and in hypertensive individuals. In addition, leptin may contribute to end-organ damage in hypertensive individuals such as left ventricular hypertrophy, retinopathy and nephropathy, independent of regulating blood pressure. Here, current knowledge about the role of leptin in the regulation of blood pressure and in the pathogenesis of arterial hypertension is presented.

摘要

瘦素是一种由白色脂肪组织分泌的16 kDa蛋白质,主要参与食物摄入和能量消耗的调节。血浆瘦素浓度与脂肪组织量成正比,在肥胖个体中显著升高。最近的研究表明,瘦素参与肥胖的心血管并发症,包括动脉高血压。急性给予瘦素对血压没有影响,这可能是因为它同时刺激交感神经系统并抵消诸如利钠作用和一氧化氮(NO)依赖性血管舒张等降压机制。相比之下,慢性高瘦素血症会升高血压,因为这些急性降压作用受损和/或出现额外的不依赖交感神经系统的升压作用,如氧化应激、NO缺乏、肾钠重吸收增强和内皮素过度产生。虽然瘦素与人类高血压之间的因果关系尚未直接得到证实,但许多临床研究表明,原发性高血压患者的血浆瘦素升高,并且在正常血压和高血压个体中,瘦素与血压之间存在显著的正相关,且与身体肥胖无关。此外,瘦素可能导致高血压个体的靶器官损害,如左心室肥厚、视网膜病变和肾病,而与血压调节无关。本文介绍了关于瘦素在血压调节和动脉高血压发病机制中作用的当前知识。

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