Hall John E, Jones Daniel W, Kuo Jay J, da Silva Alexandre, Tallam Lakshmi S, Liu Jiankang
Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216-4505, USA.
Curr Hypertens Rep. 2003 Oct;5(5):386-92. doi: 10.1007/s11906-003-0084-z.
Excess weight gain is a major cause of increased blood pressure in most patients with essential hypertension, and also greatly increases the risk for renal disease. Obesity raises blood pressure by increasing renal tubular reabsorption, impairing pressure natriuresis, causing volume expansion due to activation of the sympathetic nervous system and renin-angiotensin system, and by physical compression of the kidneys, especially when visceral obesity is present. The mechanisms of sympathetic nervous system activation in obesity may be due, in part, to hyperleptinemia that stimulates the hypothalamic pro-opiomelanocortin pathway. With prolonged obesity, there may be a gradual loss of nephron function that worsens with time and exacerbates hypertension. Weight reduction is an essential first step in the management of obesity hypertension and renal disease. Special considerations for the obese patient, in addition to adequately controlling the blood pressure, include correction of the metabolic abnormalities and protection of the kidneys from further injury.
体重过度增加是大多数原发性高血压患者血压升高的主要原因,也会大大增加患肾病的风险。肥胖通过增加肾小管重吸收、损害压力性利钠作用、因交感神经系统和肾素-血管紧张素系统激活导致血容量扩张以及对肾脏的物理压迫(尤其是存在内脏肥胖时)来升高血压。肥胖中交感神经系统激活的机制可能部分归因于刺激下丘脑阿片促黑激素皮质素原途径的高瘦素血症。随着肥胖时间延长,可能会逐渐出现肾单位功能丧失,且会随着时间恶化并加重高血压。减轻体重是肥胖相关性高血压和肾病管理的关键第一步。对于肥胖患者,除了充分控制血压外,特殊考虑因素还包括纠正代谢异常以及保护肾脏免受进一步损伤。