Birkenhäger W H, DeLeeuw P W
Hypertension. 1983 Sep-Oct;5(5 Pt 2):III31-5. doi: 10.1161/01.hyp.5.5_pt_2.iii31.
This overview is concerned with the causes of nonresponsiveness to the hypotensive action of beta-adrenergic blocking drugs. The overall hemodynamic response, i.e., a secondary decrease in peripheral vascular resistance, is unrelated to the primary decrease in cardiac output. The reduction in vascular resistance may be triggered by mechanisms residing in the central nervous system, the arterial baroreceptor area, or the prejunctional beta-receptor. None of these mechanisms seem to be entirely responsible. Studies in responders vs nonresponders tend to equate nonresponsiveness with alpha-adrenoceptor-mediated vasoconstriction. Although circulating catecholamines are relatively poor indices of sympathetic activity, studies focusing on the renal-neural area appear to show clearly differential profiles between responders and nonresponders. Such findings, in relation to experimental data on the renal nerves as selective neural amplifiers, may provide a renewed interpretation of the centrally mediated hypotensive mechanism of beta-adrenergic blockade.
本综述关注的是对β-肾上腺素能阻断药物降压作用无反应的原因。整体血液动力学反应，即外周血管阻力的继发性降低，与心输出量的原发性降低无关。血管阻力的降低可能由中枢神经系统、动脉压力感受器区域或突触前β受体中的机制触发。这些机制似乎都不能完全对此负责。对有反应者与无反应者的研究倾向于将无反应等同于α-肾上腺素能受体介导的血管收缩。尽管循环儿茶酚胺相对不能很好地反映交感神经活动，但聚焦于肾神经区域的研究似乎清楚地显示了有反应者与无反应者之间的不同特征。与关于肾神经作为选择性神经放大器的实验数据相关的这些发现，可能为β-肾上腺素能阻断的中枢介导降压机制提供新的解释。
