Iseki K
Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Am J Hypertens. 1990 Aug;3(8 Pt 2):238S-240S. doi: 10.1093/ajh/3.8.238.
Norepinephrine blood pressure reactivity is reduced in uremia, an effect attributed to excess parathyroid hormone (PTH). Most, but not all, animal and human studies support the theory that high PTH levels diminish the pressor response to norepinephrine. In hemodialysis patients in whom norepinephrine infusion tests were performed to determine the effect of parathyroidectomy on vascular responsiveness, the vascular response to norepinephrine (100 ng/kg/min) improved significantly (11.3 +/- 1.3 mm Hg before and 17.5 +/- 2.4 mm Hg after parathyroidectomy; P less than .01). Excess parathyroid hormone appears to play an active role in reduced vascular responsiveness to norepinephrine, although the mechanisms of this effect are unknown.
尿毒症患者去甲肾上腺素血压反应性降低，这种效应归因于甲状旁腺激素（PTH）过多。大多数（但并非全部）动物和人体研究支持这样的理论，即高PTH水平会减弱对去甲肾上腺素的升压反应。在进行去甲肾上腺素输注试验以确定甲状旁腺切除对血管反应性影响的血液透析患者中，对去甲肾上腺素（100 ng/kg/分钟）的血管反应显著改善（甲状旁腺切除术前为11.3±1.3 mmHg，术后为17.5±2.4 mmHg；P＜0.01）。甲状旁腺激素过多似乎在降低血管对去甲肾上腺素的反应性中起积极作用，尽管这种效应的机制尚不清楚。
