NEURAL CONTROL OF RENAL FUNCTION

所提出的研究的总体目标是检验这一假设 肾神经是重要的传入和传出神经 用于调节正常人的几种肾功能的控制系统 和病理条件。 我们之前的工作已经发现 传出肾交感神经活动作为一个重要的最终共同点 途径介导水肿形成的肾钠潴留增加 states. 具体目的是：（1）衡量相对贡献 心肺与窦主动脉压力感受器的增加， 传出肾交感神经活动和肾钠潴留 实验性心力衰竭大鼠 （2）测量心肺功能的相对贡献 和窦主动脉与肝内压力感受器的增加， 传出肾交感神经活动和肾钠潴留 实验性胆汁性肝硬化大鼠模型 结扎，（3）测量心肺功能的相对贡献 窦主动脉压力感受器与肾感觉感受器 传出肾交感神经活动和肾钠增加 阿霉素肾病综合征大鼠尿潴留 局 肾钠的各种实验模型 滞留和水肿的形成是很好的特征，并建立在 实验室 对于特定目标1-3，血液动力学测量和 电生理技术（单纤维传入和传出 神经纤维记录）将用于测量 各种假定的反射站，以增加输出肾 交感神经活动和肾钠潴留观察 模型 这些研究将有助于更清楚地界定 传出肾反射控制的病理生理学改变 在这些临床相关的肾脏模型中的交感神经活动 钠潴留和水肿形成。

The overall objective of the poposed research is to test the hypothesis that the renal nerves represent an important afferent and efferent control system for the regulation of several renal functions in normal and pathological conditions. Our previous work has identified increased efferent renal sympathetic nerve activity as an important final common pathway mediating the increased renal-sodium retention of edema forming states. The specific aims are: (1) to measure the relative contribution of cardiopulmonary versus sinoaortic baroreceptors to the increase in efferent renal sympathetic nerve activity and renal sodium retention in rats with experimental congestive heart failure due to myocardial infarction, (2) to measure the relative contribution of cardiopulmonary and sinoaortic versus intrahepatic baroreceptors to the increase in efferent renal sympathetic nerve activity and renal sodium retention in rats with experimental biliary cirrhosis due to common bile duct ligation, (3) to measure the relative contribution of cardiopulmonary and sinoaortic baroreceptors versus renal sensory receptors to the increase in efferent renal sympathetic nerve activity and renal sodium retention in rats with experimental nephrotic syndrome due to adriamycin administration. The various experimental models of renal sodium retention and edema formation are well characterized and established in the laboratory. For specific aims 1-3, hemodynamic measurements and electrophysiological techniques (single fiber afferent and efferent nerve fiber recording) will be used to measure the contribution of various putative reflex stations to the increase in efferent renal sympathetic nerve activity and renal sodium retention observed in the models. These studies will serve to more clearly define the pathophysiological alterations in reflex control of efferent renal sympathetic nerve activity in these clinically relevant models of renal sodium retention and edema formation.