Manger W M, Frohlich E D, Gifford R W, Dustan H P
J Clin Pharmacol. 1976 Feb-Mar;16(2-3):129-41. doi: 10.1002/j.1552-4604.1976.tb02394.x.
Infusion of NE in seven normal subjects and 13 patients with essential or renal hypertension caused a pronounced initial rise of systolic pressure in only seven hypertensives and one normotensive. This hyperresponsiveness was not a constant finding in essential or renal hypertensives but usually occurred in patients with highest preinfusion pressures. In some of the latter, following the pronounced rise in pressure when NE infusion was started (0.05 mug/kg/min), pressure did not increase further (probably due to reflexly reduced cardiac output) despite progressively increasing the infusion rate to 0.1 and 0.2 mug/kg/min. Hyperresponsiveness could not be attributed to increased NE concentrations at receptor sites since it was not significantly correlated with elevations of NE plasma concentrations; in some essential hypertensives, mild pressure increases occurred despite marked elevations of arterial plasma NE. Since hyperresponsiveness occurred in some patients with essential and some with renal hypertension, it could not be used to differentiate these two groups of hypertensives. The mechanism for hyperresponsiveness remains unclear but may be better explained by vascular structure alterations than by hyperreactive vascular smooth muscle per se; however, a combination of these factors could participate. During NE infusion, reflex bradycardia was associated with elevated pressure and was slightly more pronounced in normotensives; this was probably related to diminished baroreflex sensitivity in essential hypertensives and due to "resetting" of their baroreceptors. During high rates of NE infusion (0.2 mu/kg/min), higher arterial plasma NE concentrations in essential hypertensives than in normotensives could result from reduction in blood flow to organs important in inactivating circulating NE; however, a defective inactivating mechanism for NE in some essential hypertensives cannot be totally excluded.
在7名正常受试者以及13名原发性高血压或肾性高血压患者中输注去甲肾上腺素（NE），仅在7名高血压患者和1名正常血压者中引起了收缩压明显的初始升高。这种高反应性在原发性高血压或肾性高血压患者中并非持续存在，而是通常发生在输注前血压最高的患者中。在其中一些患者中，当开始输注NE（0.05微克/千克/分钟）时血压明显升高后，尽管将输注速率逐渐提高至0.1和0.2微克/千克/分钟，血压并未进一步升高（可能是由于心输出量反射性降低）。高反应性不能归因于受体部位NE浓度的增加，因为它与血浆NE浓度的升高没有显著相关性；在一些原发性高血压患者中，尽管动脉血浆NE明显升高，但血压仅轻度升高。由于原发性高血压患者和肾性高血压患者中均有部分出现高反应性，因此它不能用于区分这两组高血压患者。高反应性的机制尚不清楚，但用血管结构改变来解释可能比单纯用血管平滑肌高反应性本身更好；然而，这些因素可能共同起作用。在输注NE期间，反射性心动过缓与血压升高相关，且在正常血压者中稍更明显；这可能与原发性高血压患者压力感受器反射敏感性降低以及其压力感受器“重置”有关。在高输注速率（0.2微克/千克/分钟）的NE输注期间，原发性高血压患者动脉血浆NE浓度高于正常血压者，这可能是由于对循环中NE灭活起重要作用的器官血流减少所致；然而，也不能完全排除一些原发性高血压患者中NE灭活机制存在缺陷的可能性。
