交感神经活性（SNA）过度增强在肥胖性高血压（OH）病的发生发展中起重要作用，抑制其过度增强是防治OH的重要策略。我们研究发现脂肪传入反射（AAR）在OH大鼠显著增强，并促进SNA的增强，但目前抵抗OH病SNA增强的内源性防御因素及其分子机制研究还比较薄弱。肾上腺髓质素（ADM）在中枢和外周广泛分布，但其研究主要集中在外周，如对动物疾病模型导致心脏、血管、肾脏等损害具有保护作用。我们预实验在OH大鼠整合SNA的重要高级中枢核团室旁核（PVN）急性给予ADM或在外周皮下给予ADM（6周），都可显著降低AAR、SNA和血压。据此，我们推测ADM可通过抑制增强的AAR来降低OH大鼠的SNA进而降低血压。本课题拟用高脂饮食诱导OH大鼠模型，主要采用电生理和分子生物学实验方法探讨ADM在中枢PVN和外周对AAR的作用及作用机制，寻找有效治疗OH病的靶点，为临床防治OH病提供策略。

The over-activated sympathetic nerve activity (SNA) plays a vital role in thepathogenesis and development of obesity-related hypertension. Inhibiting the sympathetic activation has become an important strategy in preventing and treating hypertension. Adipose afferent reflex (AAR) is enhanced in obesity hypertension rats, which plays an important role in the sympathetic activation of these rats. However, it is poor in the research of endogenous defensive factors and their relative mechanisms in the enhancd SNA in OH. Adenomedullin (ADM) has a wide distribution and various biological functions both in peripheral tissues and the central nervous system. However, its research mainly concentrates on the periphery. At present, our preliminary experiment showed that ADM in the paraventricular nucleus (PVN, an important central nucleus for integrating SNA) or peripheral application of ADM significantly lowered AAR, SNA and blood pressure (BP) in OH rats. Accordingly, we speculate that ADM lowers SNA via the inhibion of the enhanced AAR in OH rats. We will use OH rats induced by high-fat diet to explore the roles and mechanisms of ADM in AAR and SNA in the PVN or peripheral application, and find effective treatment ways and targets for clinical prevention and treatment of OH.