Grassi G, Seravalle G, Dell'Oro R, Turri C, Bolla G B, Mancia G
Clinica Medica, University of Milano-Bicocca, Ospedale San Gerardo, Monza, Milan, Italy.
Hypertension. 2000 Oct;36(4):538-42. doi: 10.1161/01.hyp.36.4.538.
Previous studies have shown that essential hypertension and obesity are both characterized by sympathetic activation coupled with a baroreflex impairment. The present study was aimed at determining the effects of the concomitant presence of the 2 above-mentioned conditions on sympathetic activity as well as on baroreflex cardiovascular control. In 14 normotensive lean subjects (aged 33. 5+/-2.2 years, body mass index 22.8+/-0.7 kg/m(2) [mean+/-SEM]), 16 normotensive obese subjects (body mass index 37.2+/-1.3 kg/m(2)), 13 lean hypertensive subjects (body mass index 24.0+/-0.8 kg/m(2)), and 16 obese hypertensive subjects (body mass index 37.5+/-1.3 kg/m(2)), all age-matched, we measured beat-to-beat arterial blood pressure (by Finapres device), heart rate (HR, by ECG), and postganglionic muscle sympathetic nerve activity (MSNA, by microneurography) at rest and during baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Blood pressure values were higher in lean hypertensive and obese hypertensive subjects than in normotensive lean and obese subjects. MSNA was significantly (P:<0.01) greater in obese normotensive subjects (49.1+/-3.0 bursts per 100 heart beats) and in lean hypertensive subjects (44.5+/-3.3 bursts per 100 heart beats) than in lean normotensive control subjects (32.2+/-2.5 bursts per 100 heart beats); a further increase was detectable in individuals with the concomitant presence of obesity and hypertension (62.1+/-3. 4 bursts per 100 heart beats). Furthermore, whereas in lean hypertensive subjects, only baroreflex control of HR was impaired, in obese normotensive subjects, both HR and MSNA baroreflex changes were attenuated, with a further attenuation being observed in obese hypertensive patients. Thus, the association between obesity and hypertension triggers a sympathetic activation and an impairment in baroreflex cardiovascular control that are greater in magnitude than those found in either of the above-mentioned abnormal conditions alone.
先前的研究表明,原发性高血压和肥胖症均具有交感神经激活并伴有压力反射功能受损的特征。本研究旨在确定上述两种情况同时存在对交感神经活动以及压力反射心血管控制的影响。在14名血压正常的瘦人受试者(年龄33.5±2.2岁,体重指数22.8±0.7kg/m²[平均值±标准误])、16名血压正常的肥胖受试者(体重指数37.2±1.3kg/m²)、13名瘦的高血压受试者(体重指数24.0±0.8kg/m²)和16名肥胖的高血压受试者(体重指数37.5±1.3kg/m²)中,所有受试者年龄匹配,我们在静息状态下以及在分别通过静脉逐步输注去氧肾上腺素和硝普钠诱导压力感受器刺激和失活的过程中,测量逐搏动脉血压(通过Finapres装置)、心率(HR,通过心电图)和节后肌肉交感神经活动(MSNA,通过微神经ography)。瘦的高血压受试者和肥胖的高血压受试者的血压值高于血压正常的瘦人和肥胖受试者。肥胖的血压正常受试者(每100次心跳49.1±3.0次爆发)和瘦的高血压受试者(每100次心跳44.5±3.3次爆发)的MSNA显著(P<0.01)高于血压正常的瘦人对照受试者(每100次心跳32.2±2.5次爆发);在肥胖和高血压同时存在的个体中可检测到进一步增加(每100次心跳62.1±3.4次爆发)。此外,在瘦的高血压受试者中,仅心率的压力反射控制受损,而在肥胖的血压正常受试者中,心率和MSNA的压力反射变化均减弱,在肥胖的高血压患者中观察到进一步减弱。因此,肥胖与高血压之间的关联引发了交感神经激活以及压力反射心血管控制受损,其程度大于上述任何一种异常情况单独出现时的程度。