交感活动增强是参与肥胖高血压(OH)病形成的重要机制，但目前对OH病交感活动增强的内源性防御因素及机制研究比较薄弱。活性肽intermedin（IMD）在中枢和外周有广泛分布并具有多种生物学功能。我们研究发现在肾性高血压大鼠下丘脑室旁核（PVN）内，IMD可以降低交感神经活性(SNA)和血压。预实验证明PVN急性给予IMD显著减弱OH大鼠的SNA,外周长期慢性给予IMD明显降低OH大鼠血压。据此，我们推测IMD 在PVN通过抑制交感活动的增强发挥降低OH大鼠血压的作用。本课题拟应用高脂饮食诱导OH大鼠模型，采用电生理学和分子生物学等技术观察PVN内源性IMD及其受体系统的表达变化，探讨PVN外源性急性给予IMD对OH大鼠SNA和血压的作用及其作用机制。比较PVN过表达IMD与外周长期慢性给予IMD对OH大鼠交感活动和血压的作用，寻找有效途径，为临床防治OH病提供新思路和实验理论依据。

The enhanced sympathetic nerve activity (SNA) is one of the important mechanisms involved in obesity-related hypertension(OH). Howevere, there are few researches on endogenous factors which inhibitit the enhancd SNA and relative mechanism in OH.Intermedin (IMD), a active peptide, has a wide distribution and various biological functions in both peripheral tissues and the central nervous system. Our study showed that IMD in the PVN inhibits SNA and attenuates hypertension in renal hypertensive rats. Preliminary experiment demonstrated that peripheral application of IMD obviously decreased blood pressure (BP) in OH rats, and central IMD application into PVN significantly lowed SNA.Accordingly, we speculate that the exogenous IMD application into PVN may low BP by inhibiting the enhanced SNA in OH rats. We will use OH rats induced by high-fat diet to observe the expression of IMD and its receptor system, the effects of exogenous IMD in PVN on SNA and BP and its related mechanisms by electrophysiology and molecular biology techniques. For the purpose of therapy, we will compare the effects of IMD by gene overexpression in the PVN with the peripheral roles of IMD on SNA and BP, find out its effective way , and provide new strategy and experimental and theoretical basis for the treatment of OH.