Rea R F, Hamdan M
Department of Internal Medicine, University of Iowa, Iowa City 52242.
Circulation. 1990 Sep;82(3):856-62. doi: 10.1161/01.cir.82.3.856.
Patients with borderline hypertension have exaggerated vascular responses to orthostatic stress produced by tilt or lower body negative pressure (LBNP). It has been suggested that 1) in the supine position, these patients have augmented activity of cardiopulmonary baroreceptors that exerts an increased restraint on sympathetic vasoconstrictor tone; 2) withdrawal of this augmented inhibitory baroreceptor activity during orthostatic stress elicits augmented reflex sympathetic vasoconstrictor outflow; and 3) augmented cardiopulmonary baroreceptor activity may be secondary to impaired arterial baroreflex mechanisms. To test these hypotheses, we recorded muscle sympathetic nerve activity from the peroneal nerve in seven borderline hypertensive subjects and seven age-, sex-, and weight-matched normotensive subjects during three levels of nonhypotensive LBNP and infusions of phenylephrine and nitroprusside. During LBNP, reductions of central venous pressure were similar in borderline hypertensive and normotensive subjects, and arterial pressure and heart rate values were unchanged. Increases of sympathetic nerve activity, however, were significantly greater in borderline hypertensive than in normotensive subjects at each level of LBNP, indicating an augmented gain of the cardiopulmonary baroreflex. To determine whether this augmentation is related to impairment of arterial baroreflexes, we measured changes of sympathetic nerve activity during increases and decreases of arterial pressure produced with infusions of intravenous phenylephrine and nitroprusside. Central venous pressure was held at control levels by LBNP during phenylephrine and saline infusion during nitroprusside. Changes of sympathetic nerve activity during alterations of arterial pressure were similar in borderline hypertensive and normotensive subjects. These data show that cardiopulmonary baroreflex control of SNA is augmented in borderline hypertensive subjects and that this augmentation does not result from an attenuation of the arterial baroreflex.
临界高血压患者对由倾斜或下体负压（LBNP）产生的直立应激有夸张的血管反应。有人提出：1）在仰卧位时，这些患者心肺压力感受器的活动增强，对交感缩血管张力施加了更大的抑制作用；2）在直立应激期间，这种增强的抑制性压力感受器活动的撤回引发了增强的反射性交感缩血管流出；3）增强的心肺压力感受器活动可能继发于动脉压力反射机制受损。为了检验这些假设，我们在三个非低血压水平的LBNP以及苯肾上腺素和硝普钠输注期间，记录了7名临界高血压受试者和7名年龄、性别和体重匹配的正常血压受试者腓总神经的肌肉交感神经活动。在LBNP期间，临界高血压受试者和正常血压受试者的中心静脉压降低相似，动脉压和心率值未改变。然而，在每个LBNP水平，临界高血压受试者的交感神经活动增加明显大于正常血压受试者，表明心肺压力反射的增益增强。为了确定这种增强是否与动脉压力反射受损有关，我们测量了静脉输注苯肾上腺素和硝普钠导致动脉压升高和降低期间交感神经活动的变化。在输注苯肾上腺素期间通过LBNP将中心静脉压维持在对照水平，在输注硝普钠期间维持在生理盐水水平。在动脉压改变期间，临界高血压受试者和正常血压受试者的交感神经活动变化相似。这些数据表明，临界高血压受试者中对交感神经活动的心肺压力反射控制增强，并且这种增强不是由动脉压力反射减弱引起的。
