Mallamaci Francesca, Cutrupi Sebastiano, Pizzini Patrizia, Tripepi Giovanni, Zoccali Carmine
CNR-IBIM, Institute of Biomedicine, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension & Division of Nephrology, Dialysis and Transplantation, Reggio Calabria - Italy.
J Nephrol. 2005 Nov-Dec;18(6):727-32.
Urotensin II (UTN) is a peptide highly conserved across species with disparate effects on the vascular system and it is currently unclear whether high plasma UTN levels play a vasculotoxic or a vasculoprotective role.
In this study, we investigated the relationship between plasma UTN and sympathetic activity and cardiac natriuretic hormones in 191 hemodialysis (HD) patients without clinical evidence of heart failure.
Plasma UTN was significantly higher in patients with end-stage renal disease (ESRD) (median: 6.5 ng/mL) than in age matched healthy subjects (median: 3.1 ng/mL) (p<0.001). On univariate analysis, UTN was inversely related to heart rate (r=-0.24), dialysis treatment duration (r=-0.27), norepinephrine (r=-0.28), neuropeptide Y (NPY) (r=-0.66), brain natriuretic peptide (BNP) (r=-0.41) and atrial natriuretic peptide (ANP) (r=-0.28) (all p<0.008). Of note, in multiple regression analyses these associations maintained strength similar to that of the corresponding unadjusted correlation coefficients.
The inverse links between UTN and neuro-hormonal factors indicate that UTN down-regulation in the presence of high sympathetic activity and high BNP could be a counter-regulatory response aimed at mitigating cardiovascular (CV) damage or that UTN itself acts as a protective factor.
尾加压素II(UTN)是一种在物种间高度保守的肽,对血管系统有不同影响,目前尚不清楚血浆中高浓度的UTN发挥的是血管毒性作用还是血管保护作用。
在本研究中,我们调查了191例无心力衰竭临床证据的血液透析(HD)患者血浆UTN与交感神经活动及心脏利钠激素之间的关系。
终末期肾病(ESRD)患者的血浆UTN水平(中位数:6.5 ng/mL)显著高于年龄匹配的健康受试者(中位数:3.1 ng/mL)(p<0.001)。单因素分析显示,UTN与心率(r=-0.24)、透析治疗时长(r=-0.27)、去甲肾上腺素(r=-0.28)、神经肽Y(NPY)(r=-0.66)、脑钠肽(BNP)(r=-0.41)及心房钠尿肽(ANP)(r=-0.28)均呈负相关(所有p<0.008)。值得注意的是,在多元回归分析中,这些关联的强度与相应的未校正相关系数相似。
UTN与神经激素因子之间的反向联系表明,在交感神经活动增强和BNP升高的情况下,UTN下调可能是一种旨在减轻心血管(CV)损伤的反调节反应,或者UTN本身就是一种保护因子。