Neural mechanisms in human obesity-related hypertension
Neural mechanisms in human obesity-related hypertension
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DOI：
10.1097/00004872-199917080-00012
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发表时间：
1999-08-01
影响因子：
4.9
通讯作者：
Esler, MD
中科院分区：
文献类型：
--
作者：
Rumantir, MS;Vaz, M;Esler, MD
目的对肥胖症中体重增加和血压升高的机制进行两种假说的检验，第一种假说认为人类肥胖症中交感神经系统活动不足是肥胖症的代谢基础。第二个假说是由Landsberg提出的，即交感神经的激活与慢性暴饮暴食和血压升高有关。这些假设并非相互排斥，因为肥胖是一种异质性疾病。设计和方法研究人员使用去甲肾上腺素同位素稀释法，在休息时测量了肾脏和心脏的全身和局部交感神经系统活动，共有86名研究志愿者，他们来自四个不同的研究对象组，有瘦的和肥胖的，有高血压的或没有高血压的人。结果瘦型高血压患者全身、心脏和肾脏的去甲肾上腺素溢出量明显高于健康瘦型志愿者，正常肥胖患者全身去甲肾上腺素溢出率正常，平均肾脏去甲肾上腺素溢出量升高（正常的两倍），心脏去甲肾上腺素溢出量减少约50%，肥胖相关性高血压患者肾脏去甲肾上腺素溢出量升高。与正常肥胖者相当，但不伴有心脏去甲肾上腺素溢出抑制，是正常肥胖者的两倍多（P < 0.05），比健康志愿者高25%。高血压肥胖者的心率也有平行升高。结论肥胖的交感神经活动不足假说现在看来是站不住脚的，因为基于去甲肾上腺素溢出的测量，整个身体的交感神经系统活动正常，肾脏的交感神经系统活动增加；心脏的低交感神经活动对总能量平衡的影响微乎其微。肥胖患者肾脏交感神经活动的增加可能是肥胖患者发生高血压的必要原因，尽管显然不是充分原因，但在正常和高血压肥胖患者中都存在。肥胖相关高血压的区别特征是没有正常肥胖患者所见的心脏交感神经流出抑制。高血压患者交感神经的变化与Landsberg假说相符，中华高血压杂志，1997,17(1):1 - 3。
Objective Two hypotheses concerning mechanisms of weight gain and of blood pressure elevation in obesity were tested, The first hypothesis is that in human obesity sympathetic nervous system underactivity is present, as a metabolic basis for the obesity. The second hypothesis, attributable to Landsberg, is that sympathetic nervous activation occurs with chronic overeating, elevating blood pressure. These are not mutually exclusive hypotheses, since obesity is a heterogeneous disorder,Design and methods Whole body and regional sympathetic nervous system activity, in the kidneys and heart, was measured at rest using noradrenaline isotope dilution methodology in a total of 86 research voluteers in four different subject groups, in lean and in obese people who either did, or did not, have high blood pressure.Results In the lean hypertensive patients, noradrenaline spillover for the whole body, and from the heart and kidneys was substantially higher than in the healthy lean volunteers, In normotensive obesity, the whole body noradrenaline spillover rate was normal, mean renal noradrenaline spillover was elevated (twice normal), and cardiac noradrenaline spillover reduced by approximately 50%, In obesity-related hypertension, there was elevation of renal noradrenaline spillover, comparable to that present in normotensive obese individuals but not accompanied by suppression of cardiac noradrenaline spillover, which was more than double that of normotensive obese individuals (P < 0.05), and 25% higher than in healthy volunteers. There was a parallel elevation of heart rate in hypertensive obese individuals.Conclusions The sympathetic underactivity hypothesis of obesity causation now looks untenable, as based on measures of noradrenaline spillover, sympathetic nervous system activity was normal for the whole body and increased for the kidneys; the low sympathetic activity in the heart would have only a trifling impact on total energy balance. The increase in renal sympathetic activity in obesity may possibly be a necessary cause for the development of hypertension in obese individuals, although clearly not a sufficient cause, being present in both normotensive and hypertensive obese individuals, The discriminating feature of obesity-related hypertension was an absence of the suppression of the cardiac sympathetic outflow seen in normotensive obese individuals. Sympathetic nervous changes in obesity-related hypertension conformed rather closely to those expected from the Landsberg hypothesis, J Hypertens 1999, 17:1125-1133 (C) Lippincott Williams & Wilkins.