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在慢性心力衰竭中,人肾脏产生C型利钠肽的能力减弱。

C-type natriuretic peptide production by the human kidney is blunted in chronic heart failure.

作者信息

Kalra Paul R, Clague Jonathan R, Coats Andrew J, Anker Stefan D, Poole-Wilson Philip A, Struthers Allan D

机构信息

Department of Clinical Cardiology, National Heart & Lung Institute, London SE3 6LY, UK.

出版信息

Clin Sci (Lond). 2009 Oct 2;118(1):71-7. doi: 10.1042/CS20090092.

DOI:10.1042/CS20090092
PMID:19450232
Abstract

CNP (C-type natriuretic peptide) is a vasodilatory peptide produced by vascular endothelium and the human heart with a short half-life. CNP has been identified within the human kidney; however, few results are available on whether the human kidney is a systemic source of CNP. The aim of the present study was to establish whether CNP is secreted by the human kidney and if synthesis is blunted in CHF (chronic heart failure). A total of 20 male subjects (age, 57+/-2 years; mean+/-S.E.M.) undergoing CHF assessment (n=13) or investigation of paroxysmal supraventricular arrhythmia (normal left ventricular function in sinus rhythm during procedure) (n=7) were recruited. Renal CNP production was determined from concomitant plasma concentrations in the aorta and renal vein. When considering all subjects, a significant step-up in plasma CNP was found from the aorta to renal vein (3.0+/-0.3 compared with 8.3+/-2.4 pg/ml respectively; P=0.0045). The mean increase in CNP was 5.3+/-2.4 pg/ml (range, -0.9 to +45.3 pg/ml). In patients with CHF, the aortic concentration was 3.3+/-0.4 pg/ml compared with a renal vein concentration of 4.3+/-0.6 pg/ml (P=0.11). In those with normal left ventricular function, the respective values were 2.5+/-0.5 and 15.7+/-6.0 pg/ml (P=0.01). In conclusion, CNP is synthesized and secreted into the circulation by the normal human kidney, where it may have paracrine actions. Net renal secretion of CNP appears to be blunted in patients with CHF.

摘要

C型利钠肽(CNP)是一种由血管内皮和人类心脏产生的具有血管舒张作用的肽,半衰期较短。已在人类肾脏中发现了CNP;然而,关于人类肾脏是否是CNP的全身来源,目前几乎没有相关研究结果。本研究的目的是确定CNP是否由人类肾脏分泌,以及在慢性心力衰竭(CHF)中其合成是否受到抑制。共招募了20名男性受试者(年龄57±2岁;均值±标准误),其中13名正在接受CHF评估,7名正在接受阵发性室上性心律失常检查(检查过程中窦性心律时左心室功能正常)。通过同时测定主动脉和肾静脉中的血浆浓度来确定肾脏CNP的产生情况。在考虑所有受试者时,发现从主动脉到肾静脉血浆CNP有显著升高(分别为3.0±0.3与8.3±2.4 pg/ml;P = 0.0045)。CNP的平均升高为5.3±2.4 pg/ml(范围为 -0.9至 +45.3 pg/ml)。在CHF患者中,主动脉浓度为3.3±0.4 pg/ml,而肾静脉浓度为4.3±0.6 pg/ml(P = 0.11)。在左心室功能正常的患者中,相应的值分别为2.5±0.5和15.7±6.0 pg/ml(P = 0.01)。总之,正常人类肾脏合成并分泌CNP进入循环,在肾脏中它可能具有旁分泌作用。CHF患者中CNP的净肾分泌似乎受到抑制。

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