Russell F D, Molenaar P, O'Brien D M
The National Heart Foundation and Prince Charles Hospital Foundation Cardiovascular Research Centre, Department of Medicine, The Prince Charles Hospital, Chermside, Queensland 4032, Australia.
Br J Pharmacol. 2001 Jan;132(1):5-9. doi: 10.1038/sj.bjp.0703811.
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 Ca(2+); 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 Ca(2+); 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.
研究了最近发现的人源肽尾加压素 II(hU-II)对人心肌收缩力和冠状动脉张力的影响。在非衰竭心脏的右心房小梁中,hU-II 引起收缩力呈浓度依赖性增加(与 9.25 mM Ca²⁺相比,pEC₅₀ = 9.5 ± 0.1;Eₘₐₓ = 31.3 ± 4.8%;n = 9),收缩持续时间无变化。在移植心脏的右心室小梁中,20 nM hU-II 使收缩力略有增加(与 9.25 mM Ca²⁺相比为 7.8 ± 1.4%;n = 4 例患者中 2 例的 3/6 组织)。在心律失常实验模型中,该肽在 9 例患者中 3 例的 26 个右心房小梁中的 3 个中引起心律失常性收缩,因此与 ET-1 相比,其引起心律失常的可能性较小。hU-II(20 nM)使 1 例患者的 7/7 组织中的张力增加(为对 90 mM KCI 反应的 17.9%),而 2 例患者的 8/8 组织中未检测到反应。hU-II 是一种强效的心脏兴奋剂,但效能较低。