ARTERIAL BARORECEPTOR CONTROL OF SALT APPETITE

点击翻译按钮获取中文摘要

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.