Cardiostimulant effects of urotensin-II in human heart in vitro
Cardiostimulant effects of urotensin-II in human heart in vitro
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DOI：
10.1038/sj.bjp.0703811
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发表时间：
2001-01-01
影响因子：
7.3
通讯作者：
O'Brien, DM
中科院分区：
文献类型：
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作者：
Russell, FD;Molenaar, P;O'Brien, DM
研究了最近鉴定的人肽尾加压素-II（hU-II）对人心肌收缩力和冠状动脉张力的影响。在来自非衰竭心脏的右心房小梁中，hU-II引起收缩力的浓度依赖性增加（PEC（50）=9.5+/-0.1; E-max= 31.3+/-4.8%，与9.25 mM Ca 2+相比; n = 9），而收缩持续时间没有变化。在来自心脏破裂的右心室小梁中，20 nM hU-II引起收缩力的小幅增加（与9.25 mM Ca 2+相比为7.8+/-1.4%; n= 3/6，来自4名患者中的2名）。在心律失常的实验模型中，该肽在来自3/9名患者的3/26个右心房小梁中引起震颤性收缩，因此比ET-1引起心律失常的可能性小。hU-II（20 nM）在来自1名患者的7/7个组织中增加张力（对90 mM KCl的响应的17.9%），在来自2名患者的8/8个组织中未检测到响应。hU-II是一种强效强心剂，但效力较低。
The effects of the recently identified human peptide urotensin-II (hU-II) were investigated on human cardiac muscle contractility and coronary artery tone. In right atrial trabeculae from non-failing hearts, hU-II caused a concentration-dependent increase in contractile force (pEC(50)=9.5+/-0.1; E-max= 31.3+/-4.8% compared to 9.25 mM Ca2+; n = 9) with no change in contraction duration. In right ventricular trabeculae from explanted hearts, 20 nM hU-II caused a small increase in contractile force (7.8+/-1.4% compared to 9.25 mM Ca2+; n= 3/6 tissues from 2 out of 4 patients). The peptide caused arrhythmic contractions in 3/26 right atrial trabeculae from 3/9 patients in an experimental model of arrhythmia and therefore has less potential to cause arrhythmias than ET-1. hU-II (20 nM) increased tone (17.9% of the response to 90 mM KCI) in 7/7 tissues from 1 patient, with no response detected in 8/8 tissues from 2 patients. hU-II is a potent cardiac stimulant with low efficacy.