Collins J, Massry S G, Campese V M
Am J Nephrol. 1985;5(2):110-3. doi: 10.1159/000166915.
Patients with chronic renal failure manifest reduced pressor response to norepinephrine (NE); this abnormality is at least partly responsible for the autonomic nervous system dysfunction observed in these patients. Since uremia is associated with increased levels of parathyroid hormone (PTH) and since PTH blunts the pressor effect of NE most likely via activation of prostaglandins, we have studied the relationship between blood levels of PTH and the reduced pressor response to NE in 17 uremic patients and we examined the effect of treatment with indomethacin on the response to NE in 9 uremic and 5 normal subjects. There was a significant negative correlation (r = -0.63, p less than 0.01) between the changes in blood pressure and the blood levels of PTH in uremic patients. Treatment with indomethacin was followed by significant improvement or normalization of the pressor response to NE in uremic patients. These data are consistent with the notion that the decreased pressor response to NE in uremia is due to increased production of prostaglandins induced by excess PTH and provide a therapeutic tool for the treatment of some of the manifestations of autonomic nervous system dysfunction in uremia.
慢性肾衰竭患者对去甲肾上腺素（NE）的升压反应降低；这种异常至少部分导致了这些患者出现自主神经系统功能障碍。由于尿毒症与甲状旁腺激素（PTH）水平升高有关，且PTH最有可能通过激活前列腺素减弱NE的升压作用，我们研究了17例尿毒症患者的PTH血药浓度与NE升压反应降低之间的关系，并观察了吲哚美辛治疗对9例尿毒症患者和5例正常受试者NE反应的影响。尿毒症患者的血压变化与PTH血药浓度之间存在显著负相关（r = -0.63，p < 0.01）。吲哚美辛治疗后，尿毒症患者对NE的升压反应显著改善或恢复正常。这些数据支持以下观点：尿毒症患者对NE升压反应降低是由于PTH过量诱导前列腺素生成增加所致，为治疗尿毒症自主神经系统功能障碍的某些表现提供了一种治疗手段。
