β2肾上腺素受体(β2-AR)是广泛分布于心肌与血管平滑肌中的重要功能受体，其基因序列存在特定的多态性位点。既往文献和我们的前期研究表明，这些多态性位点所对应的氨基酸变异将导致心肌细胞收缩力及血管平滑肌反应性的改变，从而在高血压的发病中起重要作用。但其如何影响心肌和血管平滑肌的功能以及机制均尚无定论。本课题拟在前期研究的基础上，进一步进行高血压临床的评估；包装四种不同表型的β2-AR腺病毒建立细胞模型，检测不同受体表型的细胞与配体的结合作用；正向、反向检测不同受体表型对心肌及血管平滑肌功能的影响，明确不同多态性的作用。通过使用肾上腺素和受体拮抗剂，活化和抑制受体进行不同受体表型对心肌及血管平滑肌功能影响的分子机制研究，并通过找寻其他参与此过程的信号转导通路。本项目的完成旨在探讨β2-AR基因不同多态位点在高血压发病中的机制，为高血压的预防和临床个体化治疗决策提供新思路。

The human ?2-adrenoceptor (?2-AR) is one of important receptors exist among myocardial and vessel smooth muscle. Based on reference papers and our previous materials, the single nucleotide polymorphisms (SNPs) of the ?2AR subtypes have recently been reported to be positional candidate genes for changes of myocardial contractility and reactions of vessel smooth muscle cells, which play an essential role of hypertension morbidity. However, the mechanisms of how the polymorphisms affect the functions of myocardial cells and vessel smooth muscle cells are still unknown. Our studies plan to investigate the following parts: firstly we estimate the clinical effects of the polymorphisms on hypertension; secondly pack four types of ?2-AR adenovirus to set cell models; thirdly we need to assay the binding effects between different types of receptors and ligands; Fourthly we assay the ways of different types of polymorphisms on functions of myocardial cells and smooth muscle cells. Beside those we try to detect the molecular mechanisms of polymorphisms on signally transduction of these cells by adrenalin and its antagonist. The aim of our studies is to investigate the mechanism of four types of ?2-AR adenovirus on hypertension and to provide new ways of prevention and therapy.