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人尾加压素Ⅱ是生长素样环状结构 11肽 ,1998年首次在人体中克隆出来。人心肌细胞、冠状动脉粥样硬化斑块及脂质沉积的平滑肌和巨噬细胞中含有丰富的尾加压素Ⅱ ,其受体GPR 14主要分布在脊髓、丘脑、黑质及心肌、血管平滑肌、动脉的内皮细胞及部分静脉的内皮细胞。人尾加压素Ⅱ可促进血管平滑肌细胞及心肌成纤维细胞分裂、增殖 ,导致心肌肥大。人尾加压素Ⅱ不但能致血管强烈收缩及痉挛 ,而且可引起一些小动脉内皮依赖性扩张。小剂量人尾加压素Ⅱ可降低外周阻力 ,增加心输出量 ,升高冠状动脉灌注压 ;大剂量则增加外周阻力 ,降低心输出量 ,抑制心肌收缩 ,增高血压 ,降低冠状动脉灌注压 ,产生心肌缺血。急性心肌梗死、稳定型心绞痛、原发性高血压、糖尿病及小儿先天性心脏病患者血浆尾加压素Ⅱ含量明显降低。因此 ,尾加压素Ⅱ及其受体作为治疗靶点可能用于一些心血管疾病的防治
Human urotensin II is an auxin-like cyclic 11 peptide that was cloned in human for the first time in 1998. Human cardiomyocytes, coronary atherosclerotic plaques and lipid deposition of smooth muscle and macrophages is rich in urotensin Ⅱ, its receptor GPR 14 mainly in the spinal cord, thalamus, substantia nigra and myocardium, vascular smooth muscle , Arterial endothelial cells and part of the vein of endothelial cells. Human Urotensin II can promote vascular smooth muscle cells and myocardial fibroblasts division, proliferation, leading to myocardial hypertrophy. Human urotensin II can not only cause strong contraction and spasm of blood vessels, but also cause endothelium-dependent dilatation of some arterioles. Small doses of human urotensin Ⅱ can reduce the peripheral resistance, increase cardiac output, increased coronary perfusion pressure; high-dose increased peripheral resistance, reduce cardiac output, inhibit myocardial contractility, increase blood pressure, reduce coronary perfusion pressure, Myocardial ischemia. Patients with acute myocardial infarction, stable angina pectoris, essential hypertension, diabetes mellitus and congenital heart disease in patients with plasma urotensin Ⅱ levels were significantly lower. Therefore, urotensin II and its receptor as a therapeutic target may be used for the prevention and treatment of some cardiovascular diseases