ARTERIAL BARORECEPTOR CONTROL OF SALT APPETITE

动脉压力感受器对盐食欲的控制

• 批准号: 2249593
• 负责人: ROBERT L THUNHORST
• 金额: $ 6.99万
• 依托单位: UNIVERSITY OF IOWA
• 依托单位国家: 美国
• 财政年份: 1994
• 资助国家: 美国
• 起止时间: 1994-12-01 至 1996-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2249593
• 关键词: aldosterone; angiotensin II; aorta; appetite; baroreceptors; baroreflex; biological models; blood pressure; blood volume; body fluids; carotid sinus; denervation; dietary sodium; diuresis; hemodynamics; hormone regulation /control mechanism; laboratory rat; neural information processing; nutrition related tag; oxytocin; renin; renin angiotensin system; salt intake; saluresis; sensory mechanism

The goal of the proposed research is to study the contributions of one set of vascular, neural sensors, i.e. arterial baroreceptors, to the expression of salt appetite in rats after extracellular fluid (ECF) depletion. Preliminary work has established that eliminating arterial baroreceptor input to the central nervous system via surgical transectio of the relevant nerves (sinoaortic baroreceptor denervation; SAD) impair salt intakes of rats tested in one widely-used experimental model of sal appetite, and an additional, newer model. This is the first direct evidence of arterial baroreceptor involvement in salt appetite. The proposed research will extend our knowledge of the role of vascular, neural mechanisms to the production of salt appetite by addressing two specific aims. The first aim is to investigate the role of arterial baroreceptors in three specific models of salt appetite that are mediate by different physiological mechanisms. Sham denervated and SAD rats wil be tested in three experimental protocols that produce unique profiles of hormone secretion, latency to ingest saline, and changes in ECF volume. These experiments will characterize the specific conditions in which sinoaortic baroreceptor denervation impairs salt intake. The second aim is to investigate the mechanisms by which arterial baroreceptor denervation impairs salt intake. Sham denervated and SAD rats will be tested after ECF volume depletion for 1) characterization of moment-to-moment arterial blood pressure and (2) measurement of plasm levels of angiotensin and aldosterone, hormones that are implicated in the initiation of salt appetite, and of oxytocin, a hormone that is implicated in the inhibition of salt appetite. These experiments will determine if the hemodynamic or endocrine consequences of sinoaortic baroreceptor denervation accounts for the impaired salt intakes of SAD rats. This research will add to our understanding of vascular, neural sensory contributions to the ingestion of sodium, a substance that both is linked to the pathogenesis of hypertension and is essential to life.

拟议研究的目标是研究一个人的贡献， 一组血管神经传感器，即动脉压力感受器， 细胞外液（ECF）后大鼠盐食欲的表达 耗尽 初步工作已经确定，消除动脉 通过手术切断向中枢神经系统的压力感受器输入 相关神经（窦主动脉压力感受器去神经支配; SAD）受损 在一个广泛使用的盐的实验模型中测试的大鼠的盐摄入量 食欲，和一个额外的，更新的模式。 这是第一次直接 动脉压力感受器参与盐食欲的证据。 的 拟议的研究将扩展我们对血管作用的认识， 神经机制，以生产盐的食欲，解决两个 明确的目标。 第一个目标是研究动脉的作用 压力感受器在三种特定的盐食欲模型中， 通过不同的生理机制。 假去神经和SAD大鼠将 在三个实验方案中进行测试， 激素分泌，摄入盐水的潜伏期以及ECF的变化 音量. 这些实验将描述特定的条件， 窦主动脉压力感受器去神经损伤盐的摄入。 的 第二个目的是研究动脉粥样硬化的机制， 压力感受器去神经损害盐的摄入。 假手术失神经支配和SAD 将在ECF容量耗尽后对大鼠进行试验，以进行1）表征 的时刻到时刻的动脉血压和（2）测量血浆 血管紧张素和醛固酮的水平，这些激素与 盐的食欲和催产素的开始，催产素是一种激素， 抑制盐的食欲。 这些实验将 确定窦主动脉的血流动力学或内分泌后果 压力感受器去神经支配导致SAD患者盐摄入受损 大鼠 这项研究将增加我们对血管，神经， 对摄入钠的感觉贡献，一种物质， 与高血压的发病机制有关，对生命至关重要。