血管紧张素Ⅱ受体(ANGⅡR)和降钙素基因相关肽受体(CGRPR)同属于G蛋白藕联受体家族。研究发现,单独激活ANGIIR或CGRPR和同时激活两受体对细胞的命运表现出不同甚至相反的作用。目前已知,CGRP受体是由降钙素受体样受体(CRLR)、受体活性修饰蛋白-l(RAMP1)、受体组分蛋白(RCP)3个组分组成。ANGⅡR和CGRPR间的相互作用可能发生在细胞膜的信号转导、细胞浆信号通路以及核内的基因转录等水平。本文综述了ANGⅡR和CGRPR在跨膜信号蛋白(如G蛋白及caveolae/caveoilins)、胞浆.胞核内信号蛋白(如NADPH氧化酶、MAPK家族)水平的相互作用,可望从心血管受体间信号整合改变的新视角来解释心血管疾病的发病机制。
The vascular peptides play a key role in the development of cardiovascular diseases. Angiotensin ll(Angll), a key effector of the reninangiotensin system (RAS), induces proliferation and transformation of vascular smooth muscle cells (VSMCs), cardiac hypertrophy and so on, is thought to underlie the cardiovascular diseases, such as hypertension and heart failure. Calcitonin gene related peptide (CGRP) is a bioactive neuropeptide released from capsaicin sensitive nervous terminal, which extensively distributes in nervous and cardiovascular system. The multiple biological effects of CGRP, such as vasolatation, inhibition of VSMC proliferation, prevention of endothelial cell ( EC ) apoptosis, promoting ECs proliferation, are suggested to be beneficial to cardiovascular system. Studies demonstrated that there arebiological interactions be tween the CGRP and Angll. It has been reported that exogenous and locally converted AngII decreases the function of CGRP nerves (release CGRP) in SHRs with age, which are related to the devel opment of chronic hypertension and activation of the neuronal AT1 receptor by Angll inhibits CGRP synthesis in the dorsal root ganglia. Interestingly, others and our researches showed that CGRP inhibits AngIIinduced proliferation and transformation ofVSMCs. Angll induces EC apoptosis which is protected by CGRP. These phenomenons suggested that there are interactions between the CGRP and AnglI in the receptor and signal pathway levels, which affect the cellular function in different cell type.