da Silva Alexandre A, do Carmo Jussara, Dubinion John, Hall John E
Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216-4505, USA.
Curr Hypertens Rep. 2009 Jun;11(3):206-11. doi: 10.1007/s11906-009-0036-3.
Obesity is recognized as a major health problem throughout the world. Excess weight is a major cause of increased blood pressure in most patients with essential hypertension and greatly increases the risk for diabetes, cardiovascular diseases, and end-stage renal disease. Although the mechanisms by which obesity raises blood pressure are not completely understood, increased renal sodium reabsorption, impaired pressure natriuresis, and volume expansion appear to play important roles. Several potential mechanisms have been suggested to contribute to altered kidney function and hypertension in obesity, including activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, as well as physical compression of the kidneys, especially when visceral obesity is present. Activation of the sympathetic nervous system in obesity may be due, in part, to hyperleptinemia and other factors secreted by adipocytes and the gastrointestinal tract, activation of the central nervous system melanocortin pathway, and baroreceptor dysfunction.
肥胖被公认为是全球主要的健康问题。超重是大多数原发性高血压患者血压升高的主要原因,并且极大地增加了患糖尿病、心血管疾病和终末期肾病的风险。尽管肥胖导致血压升高的机制尚未完全明确,但肾钠重吸收增加、压力性利钠受损和血容量扩张似乎起着重要作用。已有几种潜在机制被认为与肥胖时肾功能改变和高血压有关,包括交感神经系统和肾素 - 血管紧张素 - 醛固酮系统的激活,以及肾脏受到物理压迫,尤其是存在内脏肥胖时。肥胖时交感神经系统的激活可能部分归因于高瘦素血症以及脂肪细胞和胃肠道分泌的其他因素、中枢神经系统黑皮质素途径的激活和压力感受器功能障碍。