C type natruiretic peptide production by the human kidney is blunted in chronic heart failure
Résumé
C-type natriuretic peptide (CNP) is a vasodilatory peptide produced by vascular endothelium and human heart with a short half-life. CNP has been identified within the human kidney. Few data are available on whether the human kidney is a systemic source of CNP. The aim of the current study was to establish whether CNP is secreted by human kidney and whether synthesis is blunted in chronic heart failure (CHF). 20 male subjects (age 57±2 years, mean±SEM) undergoing CHF assessment (n=13) or investigation of paroxysmal supraventricular arrhythmia (n=7, normal left ventricular function, in sinus rhythm during procedure) were recruited. Renal CNP production was determined from concomitant plasma concentration in aorta and renal vein. When considering all subjects, a significant step-up in plasma CNP was found from aorta to renal vein (3.0±0.3 vs 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, aortic concentration was 3.3±0.4 pg/mL as compared with renal vein concentration 4.3±0.6 pg/mL (p=0.11). In those with normal left ventricular function the respective values were 2.5±0.5 pg/mL and 15.7±6.0pg/mL (p=0.01). CNP is synthesised and secreted into the circulation by the normal human kidney, where it may have paracrine actions. Net renal secretion of CNP appears blunted in patients with CHF.
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