Rumantir M S, Vaz M, Jennings G L, Collier G, Kaye D M, Seals D R, Wiesner G H, Brunner-La Rocca H P, Esler M D
Baker Medical Research Institute and Alfred Baker Medical Unit, Alfred Hospital, Melbourne, Australia.
J Hypertens. 1999 Aug;17(8):1125-33. doi: 10.1097/00004872-199917080-00012.
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.
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.
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.
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.
对有关肥胖症中体重增加机制和血压升高机制的两种假说进行了验证。第一种假说是，在人类肥胖症中存在交感神经系统活动不足，这是肥胖症的代谢基础。第二种假说由兰兹伯格提出，即慢性暴饮暴食会导致交感神经激活，从而使血压升高。由于肥胖症是一种异质性疾病，所以这两种假说并非相互排斥。
使用去甲肾上腺素同位素稀释法，对四个不同受试组（包括体重正常者和肥胖者，其中肥胖者又分为有高血压和无高血压两类）的总共86名研究志愿者在静息状态下测量了全身及肾脏和心脏等局部的交感神经系统活动。
在体重正常的高血压患者中，全身以及心脏和肾脏的去甲肾上腺素溢出量显著高于健康的体重正常志愿者。在血压正常的肥胖者中，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（为正常的两倍），而心脏去甲肾上腺素溢出量降低约50%。在与肥胖相关的高血压患者中，肾脏去甲肾上腺素溢出量升高，与血压正常的肥胖个体中的情况相当，但并未伴随心脏去甲肾上腺素溢出量的抑制，其心脏去甲肾上腺素溢出量是血压正常的肥胖个体的两倍多（P<0.05），且比健康志愿者高25%。高血压肥胖个体的心率也相应升高。
基于去甲肾上腺素溢出量的测量结果，肥胖症成因的交感神经系统活动不足假说现在看来难以成立，因为全身交感神经系统活动正常，肾脏的交感神经系统活动增加；心脏交感神经活动较低对总能量平衡的影响微不足道。肥胖症中肾脏交感神经活动的增加可能是肥胖个体患高血压的必要原因，尽管显然不是充分原因，因为血压正常和高血压肥胖个体中均存在这种情况。与肥胖相关的高血压的区别特征是不存在血压正常的肥胖个体中所见的心脏交感神经输出抑制。与肥胖相关的高血压中的交感神经变化与兰兹伯格假说所预期的情况相当吻合。
