RENAL AND CARDIOVASCULAR MECHANISMS OF HYPERTENSION IN OBESITY
RENAL AND CARDIOVASCULAR MECHANISMS OF HYPERTENSION IN OBESITY
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DOI：
10.1161/01.hyp.23.3.381
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发表时间：
1994-03-01
期刊：
影响因子：
8.3
通讯作者：
HALL, JE
中科院分区：
文献类型：
--
作者：
HALL, JE
在所有形式的高血压，包括人类原发性高血压，血压钠尿重置为高血压；由于人类原发性高血压是一种异质性疾病，可能有多种神经体液和肾内原因导致血压异常尿钠和血压升高。体重增加被认为是原发性高血压的一个重要因素，尽管肥胖与肾功能改变和高血压之间的联系机制尚未完全阐明。在肥胖的狗和人类中，压力性尿钠向高血压的转变似乎主要是由于肾小管重吸收增加，因为肾小球滤过率和肾血浆流量比正常情况下增加。肥胖引起肾小管重吸收增加和高血压的原因有多种，包括胰岛素抵抗和高胰岛素血症、交感神经和肾素血管紧张素系统的激活以及肾脏本身的物理变化。支持胰岛素抵抗-高胰岛素血症在肥胖和高血压之间的联系主要是从急性和流行病学研究中推断出来的，这些研究显示胰岛素和血压之间存在相关性。最近的研究表明，慢性高胰岛素血症，与肥胖中发现的相似，不能解释狗或人类的肥胖高血压。交感神经系统的激活可能在肥胖引起的高血压中起作用，并且有证据表明肾内物理力的改变是由肾髓质的组织学改变引起的。这些异常在改变肾功能和肥胖患者血压升高中的定量重要性仍有待确定，但这是了解人类原发性高血压的一个重要研究领域。
In all forms of hypertension, including human essential hypertension, pressure natriuresis is reset to higher blood pressures; Because human essential hypertension is a heterogeneous disease, it is likely that there are multiple neurohumoral and intrarenal causes of abnormal pressure natriuresis and increased blood pressure. Weight gain is recognized to be an important contributor to essential hypertension, although the mechanisms that link obesity with altered renal function and high blood pressure have not been fully elucidated. In obese dogs and humans, the shift of pressure natriuresis to higher blood pressures appears to be due mainly to increased tubular reabsorption, as glomerular filtration rate and renal plasma flow are increased compared with normal. Multiple causes of increased tubular reabsorption and hypertension in obesity have been postulated, including insulin resistance and hyperinsulinemia, activation of the sympathetic nervous and renin-angiotensin systems, and physical changes within the kidney itself. Support for the insulin resistance-hyperinsulinemia link between obesity and hypertension has been inferred mainly from acute and epidemiologic studies showing a correlation between insulin and blood pressure. Recent studies suggest that chronic hyperinsulinemia, comparable to that found in obesity, cannot account for obesity hypertension in dogs or humans. Activation of the sympathetic nervous system may play a role in obesity-induced hypertension, and there is evidence for a role of altered intrarenal physical forces caused by histological changes within the renal medulla. The quantitative importance of each of these abnormalities in altering renal function and raising blood pressure in obesity remains to be determined but is an important area of research for understanding human essential hypertension.