Grassi G, Cattaneo B M, Seravalle G, Lanfranchi A, Mancia G
Cattedra di Medicina Interna, Ospedale S.Gerardo dei Tintori, Monza, Università di Milano, Italy.
Hypertension. 1998 Jan;31(1):68-72. doi: 10.1161/01.hyp.31.1.68.
Studies performed in experimental animals and in humans have documented that high blood pressure markedly impairs baroreceptor control of heart rate. Whether a similar impairment also characterizes baroreceptor control of sympathetic activity modulating peripheral vasomotor tone is still unknown. In 28 untreated essential hypertensive subjects [14 of moderate and 14 of more severe degree, age 51.6+/-2.4 and 52.6+/-2.1 years (mean+/-SEM)] and in 13 untreated secondary hypertensives (renovascular or pheochromocytoma, age 50.1+/-4.6 years), we measured beat-to-beat arterial blood pressure (finger photoplethysmographic device), heart rate (electrocardiogram), and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Data were compared with those obtained in 15 age-matched normotensive control subjects. Muscle sympathetic nerve activity (bursts per 100 heart beats) showed a progressive and significant (P<.01) increase from normotension (40.3+/-3.3) to moderate (55.6+/-4.1) and more severe essential hypertension (68.2+/-4.1), paralleling the progressive increase in blood pressure values. In contrast, muscle sympathetic nerve activity was not increased in secondary hypertensives (40.5+/-6.7) despite blood pressure values similar to or even greater than those of severe essential hypertensives. In both essential and secondary hypertensives, baroreceptor-heart rate control was displaced toward elevated blood pressure values and markedly impaired compared with normotensive subjects (average reduction, 38.5%). In contrast, the sympathoinhibitory and sympathoexcitatory responses to baroreceptor stimulation and deactivation were displaced toward elevated blood pressure values but similar in all groups. Thus, sympathetic activation characterizes essential but not secondary hypertension. Regardless of its nature, however, hypertension is not accompanied by an impairment of baroreceptor modulation of sympathetic activity.
在实验动物和人类中进行的研究已证明，高血压会显著损害压力感受器对心率的控制。压力感受器对调节外周血管运动张力的交感神经活动的控制是否也存在类似损害仍不清楚。在28名未经治疗的原发性高血压患者[14名中度和14名重度患者，年龄分别为51.6±2.4岁和52.6±2.1岁（平均值±标准误）]以及13名未经治疗的继发性高血压患者（肾血管性或嗜铬细胞瘤，年龄50.1±4.6岁）中，我们分别在静息状态以及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期间，测量逐搏动脉血压（手指光电容积描记装置）、心率（心电图）和节后肌肉交感神经传出活动（微神经ography）。将数据与15名年龄匹配的血压正常对照受试者的数据进行比较。肌肉交感神经活动（每100次心跳的爆发次数）显示，从血压正常（40.3±3.3）到中度（55.6±4.1）和重度原发性高血压（68.2±4.1），其呈逐渐且显著（P<0.01）增加，与血压值的逐渐升高平行。相比之下，继发性高血压患者（40.5±6.7）的肌肉交感神经活动并未增加，尽管其血压值与重度原发性高血压患者相似甚至更高。在原发性和继发性高血压患者中，压力感受器 - 心率控制均向血压升高值偏移，且与血压正常受试者相比明显受损（平均降低38.5%）。相比之下，对压力感受器刺激和失活的交感抑制和交感兴奋反应向血压升高值偏移，但在所有组中相似。因此，交感神经激活是原发性高血压而非继发性高血压的特征。然而，无论其性质如何，高血压均不伴有压力感受器对交感神经活动调节的损害。
