Koomans Hein A, Blankestijn Peter J, Joles Jaap A
Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands.
J Am Soc Nephrol. 2004 Mar;15(3):524-37. doi: 10.1097/01.asn.0000113320.57127.b9.
Sympathetic hyperactivity plays an important and distinct role in hypertension associated with chronic renal failure (CRF). Renal ischemia, elevated angiotensin II, and suppressed brain nitric oxide (NO) all stimulate sympathetic activity. Evidence is accumulating for a role of sympathetic hyperactivity in renal and cardiac damage in patients with CRF. Decreased NO availability and increased oxidative stress, characteristic in CRF patients, seem to sensitize target organs for damaging actions of sympathetic hyperactivity. Fortunately, sympatholytic agents can slow down progression of renal and cardiac dysfunction. Angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists suppress sympathetic activity, but complete elimination of the effect of sympathetic hyperactivity can be obtained only with specific adrenergic blockers. However, this important therapeutic option is grossly neglected, painfully illustrated by the unwillingness to treat CRF patients with beta-blockers, even if they have had a myocardial infarction. After discussion of mechanisms and effects of the sympathetic hyperactivity, a case is made for increased application of specific adrenergic blockers in patients with CRF.
交感神经过度活跃在慢性肾衰竭（CRF）相关的高血压中起着重要且独特的作用。肾缺血、血管紧张素II升高以及脑一氧化氮（NO）受抑制均会刺激交感神经活动。越来越多的证据表明，交感神经过度活跃在CRF患者的肾脏和心脏损伤中发挥作用。CRF患者的典型特征是NO可用性降低和氧化应激增加，这似乎使靶器官对交感神经过度活跃的损伤作用更加敏感。幸运的是，抗交感神经药物可以减缓肾脏和心脏功能障碍的进展。血管紧张素转换酶抑制剂或血管紧张素II受体拮抗剂可抑制交感神经活动，但只有使用特定的肾上腺素能阻滞剂才能完全消除交感神经过度活跃的影响。然而，这一重要的治疗选择却被严重忽视，不愿用β受体阻滞剂治疗CRF患者就痛苦地说明了这一点，即使他们曾发生过心肌梗死。在讨论了交感神经过度活跃的机制和影响后，本文提出应增加特定肾上腺素能阻滞剂在CRF患者中的应用。
