BARORECEPTORS AND HORMONES IN THIRST AND SALT APPETITE

描述：本提案建立在研究者先前的 液体相关的传入信号和中枢神经系统的研究 处理. 拟议的研究将采用最近开发的模型 在大鼠中，允许研究相互作用的激素 （血管紧张素）和神经（动脉和心肺压力感受器） 控制低血容量性口渴和盐食欲的传入信号。 初步实验表明， 动脉压[AP]分别促进和抑制水 由脑室内血管紧张素II引起的饮酒。 第1部分 建议检查动脉压的调节作用[AP]对 急性钠缺乏后产生盐食欲。 第二 一系列初步实验表明，缺乏动脉的大鼠 压力感受器输入到大脑后，手术切除相关的 神经（即， 颈动脉窦和主动脉弓的去神经支配 压力感受器）在两个实验模型中的盐摄入量受损， 钠缺乏引起的盐食欲，主要依赖于行动， 产生盐的食欲。 第二部分扩大 这条调查线的贡献，另一套 血管神经传感器，即心肺压力感受器， 钠缺乏后的食欲。 最近，第三系列 研究表明肾神经与盐的产生有关 细胞外液耗尽后食欲不振。 第三部分 建议将继续这项研究，以确定是否肾传入或 传出神经为这种现象提供了基础。

DESCRIPTION: The present proposal builds upon the investigator's prior investigations of fluid-related afferent signaling and central processing. The proposed research will employ recently developed models in the rat that permit the investigation of interactive hormonal (angiotensin) and the neural (arterial and cardiopulmonary baroreceptor) afferent signals that control hypovolemic thirst and salt appetite. Preliminary experiments demonstrate that decreases and increases in arterial pressure [AP] respectively facilitate and inhibit water drinking induced by intraventricular angiotensin II. Part 1 of the proposal examines modulatory effects of arterial pressure [AP] on the generation of salt appetite following acute sodium depletion. A second series of preliminary experiments demonstrate that rats lacking arterial baroreceptor input to the brain after surgical removal of the relevant nerves (i.e., denervation of the carotid sinus and aortic arch baroreceptors) have impaired salt intakes in two experimental models of sodium depletion-induced salt appetite that rely largely on the actions of ANG II to produce the salt appetite. Part 2 of this proposal extend this line of investigation to the contributions of another set of vascular neural sensors, i.e. cardiopulmonary baroreceptors, to the salt appetite that follows sodium depletion. A recent, third series of studies has implicated the renal nerves in the production of salt appetite following extracellular fluid depletion. Part 3 of this proposal will continue this research to determine if renal afferent or efferent nerves provide the basis for this phenomenon.