Role of leptin in blood pressure regulation and arterial hypertension

被引:11
作者
Beltowski, Jerzy [1 ]
机构
[1] Med Univ Lublin, Dept Pathophysiol, PL-20090 Lublin, Poland
关键词
arterial hypertension; leptin; leptin resistance; Na+; K+-ATPase; natriuresis; nitric oxide; oxidative stress;
D O I
暂无
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
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. J Hypertens 24:789-801 (c) 2006 Lippincott Williams & Wilkins.
引用
收藏
页码:789 / 801
页数:13
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