ARTERIAL BARORECEPTOR CONTROL OF SALT APPETITE

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，到 细胞外液(ECF)对大鼠食盐量的影响 耗尽。初步研究表明，消除动脉 压力感受器通过手术横断进入中枢神经系统 相关神经(窦主动脉压力感受器去神经；SAD)受损 在一种广泛使用的SAL实验模型上测试大鼠的食盐摄入量 胃口，以及一个额外的，较新的型号。这是第一次直接 动脉压力感受器参与食盐摄取的证据。这个 拟议中的研究将扩大我们对血管作用的了解， 通过解决两个问题实现食盐产生的神经机制 明确的目标。第一个目的是研究动脉的作用 调节食盐量的三种特定模型中的压力感受器 通过不同的生理机制。假手术失神经和SAD大鼠 在产生独特配置文件的三个实验协议中进行测试 激素分泌、摄入生理盐水的潜伏期和ECF的变化 音量。这些实验将表征特定条件下的 去窦主动脉压力感受器神经会损害盐的摄入量。这个 第二个目标是研究动脉 压力感受器失神经会损害盐的摄入量。假失神经和SAD 在ECF容量耗尽后，将对大鼠进行测试，以进行1)表征 和(2)血浆的测量 血管紧张素和醛固酮水平，这两种激素与 食盐和催产素的开始，催产素是一种 牵涉到抑制食盐的食欲。这些实验将 确定窦主动脉的血流动力学或内分泌后果 压力感受器失神经是SAD盐摄入量受损的原因 老鼠。这项研究将增加我们对血管、神经 感官对钠摄取的贡献，钠是一种物质，既 与高血压的发病机制有关，是生命所必需的。

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.