Hogikyan R V, Supiano M A
Department of Internal Medicine, University of Michigan, Ann Arbor.
J Clin Invest. 1993 Apr;91(4):1429-35. doi: 10.1172/JCI116347.
The purpose of this study was to test the hypothesis that there is homologous upregulation of arterial alpha-adrenergic responsiveness during suppression of sympathetic nervous system (SNS) activity in humans. 10 subjects (19-28 yr) were studied during placebo and when SNS activity was suppressed by guanadrel. Changes in forearm blood flow (FABF) mediated by the intraarterial infusion of norepinephrine (NE), angiotensin II (AII), and phentolamine were measured by plethysmography. During guanadrel compared with placebo, plasma NE levels (1.28 +/- 0.09-0.85 +/- 0.06 nM; P = 0.0001) and the extra vascular NE release rate derived from [3H]NE kinetics were lower (7.1 +/- 0.7-4.0 +/- 0.2 nmol/min per m2; P = 0.0004), suggesting suppression of SNS activity. During guanadrel, there was increased sensitivity in the FABF response to NE (analysis of variance P = 0.03). In contrast, there was no difference in the FABF response to AII (analysis of variance P = 0.81), suggesting that the upregulation observed to NE was homologous. The increase in FABF during phentolamine was similar during guanadrel compared with placebo (guanadrel: 141 +/- 37 vs. placebo; 187 +/- 27% increase; P = 0.33), suggesting that there was at least partial compensation to maintain constant endogenous arterial alpha-adrenergic tone. We conclude that there is homologous upregulation of arterial alpha-adrenergic responsiveness in humans when SNS activity is suppressed by guanadrel.
在人类交感神经系统（SNS）活动受到抑制期间，动脉α-肾上腺素能反应性存在同源上调。对10名受试者（19 - 28岁）在服用安慰剂时以及胍乙啶抑制SNS活动时进行了研究。通过体积描记法测量动脉内输注去甲肾上腺素（NE）、血管紧张素II（AII）和酚妥拉明介导的前臂血流量（FABF）变化。与安慰剂相比，胍乙啶治疗期间，血浆NE水平（1.28±0.09 - 0.85±0.06 nM；P = 0.0001）以及由[3H]NE动力学得出的血管外NE释放率较低（7.1±0.7 - 4.0±0.2 nmol/min per m2；P = 0.0004），提示SNS活动受到抑制。在胍乙啶治疗期间，FABF对NE的反应敏感性增加（方差分析P = 0.03）。相比之下，FABF对AII的反应无差异（方差分析P = 0.81），表明观察到的对NE的上调是同源的。与安慰剂相比，胍乙啶治疗期间酚妥拉明引起的FABF增加相似（胍乙啶：141±37 vs. 安慰剂；增加187±27%；P = 0.33），提示至少存在部分代偿以维持内源性动脉α-肾上腺素能张力恒定。我们得出结论，当胍乙啶抑制SNS活动时，人类动脉α-肾上腺素能反应性存在同源上调。
