Sharma A M, Engeli S, Pischon T
Department of Nephrology and Hypertension, Franz-Volhard-Klinik, Universitätsklinikum Charité, Humboldt-University zu Berlin, Wiltbergstr. 50, 13125 Berlin, Federal Republic of Germany.
Curr Hypertens Rep. 2001 Apr;3(2):152-6. doi: 10.1007/s11906-001-0030-x.
Hypertension develops in almost 60% of obese individuals. Apart from the recent observation of obesity-associated structural changes in kidney structure that may lead to enhanced tubular sodium reabsorbtion, reports of paracrine and hormonal factors derived from adipose tissue have prompted speculations about the role of adipose tissue in the pathophysiology of obesity-induced hypertension. We summarize recent data on leptin's sympathoexcitatory actions, the possible influence of adipose tissue on atrial natriuretic peptide levels, and the formation of vasoactive substances, such as angiotensin II and nonesterified fatty acids, by adipocytes. The mechanisms discussed herein may contribute to the typical findings in obesity-induced hypertension, including volume expansion, sodium retention, enhanced sympathetic nervous system activity, increased activity of the systemic renin-angiotensin system, low atrial natriuretic peptide levels, and disturbed glucose and insulin metabolism. Together, these data strengthen the hypothesis that adipose tissue is potentially a major regulator of cardiovascular-renal function.
近60%的肥胖个体患有高血压。除了最近观察到肥胖相关的肾脏结构变化可能导致肾小管钠重吸收增强外，来自脂肪组织的旁分泌和激素因子的报道引发了人们对脂肪组织在肥胖诱导的高血压病理生理学中作用的猜测。我们总结了有关瘦素的交感神经兴奋作用、脂肪组织对心房利钠肽水平的可能影响以及脂肪细胞形成血管活性物质（如血管紧张素II和非酯化脂肪酸）的最新数据。本文讨论的机制可能导致肥胖诱导的高血压的典型表现，包括容量扩张、钠潴留、交感神经系统活动增强、全身肾素-血管紧张素系统活性增加、心房利钠肽水平降低以及葡萄糖和胰岛素代谢紊乱。总之，这些数据强化了脂肪组织可能是心血管-肾功能主要调节因子的假说。
