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心血管调节中的尾加压素II

Urotensin II in cardiovascular regulation.

作者信息

Russell Fraser D

机构信息

School of Health and Sport Sciences, Faculty of Science, Health and Education, University of the Sunshine Coast, Sippy Downs, Queensland, Australia.

出版信息

Vasc Health Risk Manag. 2008;4(4):775-85. doi: 10.2147/vhrm.s1983.

DOI:10.2147/vhrm.s1983
PMID:19065995
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2597773/
Abstract

Cardiovascular function is modulated by neuronal transmitters, circulating hormones, and factors that are released locally from tissues. Urotensin II (UII) is an 11 amino acid peptide that stimulates its' obligatory G protein coupled urotensin II receptors (UT) to modulate cardiovascular function in humans and in other animal species, and has been implicated in both vasculoprotective and vasculopathic effects. For example, tissue and circulating concentrations of UII have been reported to increase in some studies involving patients with atherosclerosis, heart failure, hypertension, preeclampsia, diabetes, renal disease and liver disease, raising the possibility that the UT receptor system is involved in the development and/or progression of these conditions. Consistent with this hypothesis, administration of UT receptor antagonists to animal models of cardiovascular disease have revealed improvements in cardiovascular remodelling and hemodynamics. However, recent studies have questioned this contributory role of UII in disease, and have instead postulated a protective effect on the cardiovascular system. For example, high concentrations of circulating UII correlated with improved clinical outcomes in patients with renal disease or myocardial infarction. The purpose of this review is to consider the regulation of the cardiovascular system by UII, giving consideration to methodologies for measurement of plasma concentrations, sites of synthesis and triggers for release.

摘要

心血管功能受神经递质、循环激素以及从组织局部释放的因子调节。尾加压素II(UII)是一种由11个氨基酸组成的肽,它刺激其特异性G蛋白偶联的尾加压素II受体(UT),从而调节人类和其他动物物种的心血管功能,并且已被证明具有血管保护和血管病变作用。例如,在一些涉及动脉粥样硬化、心力衰竭、高血压、先兆子痫、糖尿病、肾脏疾病和肝脏疾病患者的研究中,已报道UII的组织和循环浓度会升高,这增加了UT受体系统参与这些疾病发生和/或进展的可能性。与该假设一致,给心血管疾病动物模型施用UT受体拮抗剂已显示出心血管重塑和血流动力学方面的改善。然而,最近的研究对UII在疾病中的这种作用提出了质疑,转而推测其对心血管系统具有保护作用。例如,高浓度的循环UII与肾脏疾病或心肌梗死患者的临床结局改善相关。本综述的目的是探讨UII对心血管系统的调节作用,同时考虑血浆浓度的测量方法、合成部位和释放触发因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adf5/2597773/48d0a31e1b35/vhrm-4-0775f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adf5/2597773/48d0a31e1b35/vhrm-4-0775f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adf5/2597773/48d0a31e1b35/vhrm-4-0775f1.jpg

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Liver Int. 2007 Nov;27(9):1232-9. doi: 10.1111/j.1478-3231.2007.01539.x.
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Urotensin II acutely increases myocardial length and distensibility: potential implications for diastolic function and ventricular remodeling.尾加压素II可急性增加心肌长度和扩张性:对舒张功能和心室重构的潜在影响。
Naunyn Schmiedebergs Arch Pharmacol. 2007 Oct;376(1-2):107-15. doi: 10.1007/s00210-007-0180-8. Epub 2007 Aug 14.
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Role of urotensin II and its receptor in health and disease.
Bioinformatic analysis and functional predictions of selected regeneration-associated transcripts expressed by zebrafish microglia.
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BMC Genomics. 2020 Dec 7;21(1):870. doi: 10.1186/s12864-020-07273-8.
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Braz J Cardiovasc Surg. 2020 Oct 1;35(5):675-682. doi: 10.21470/1678-9741-2019-0470.
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The roles of potassium channels in contractile response to urotensin-II in mercury chloride induced endothelial dysfunction in rat aorta.钾通道在氯化汞诱导的大鼠主动脉内皮功能障碍中对尾加压素II收缩反应中的作用。
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The Role of Cardiac Side Population Cells in Cardiac Regeneration.心脏侧群细胞在心脏再生中的作用。
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