FOREBRAIN AND HINDBRAIN MECHANISMS OF SALT APPETITE

盐食欲的前脑和后脑机制

• 批准号: 6477077
• 负责人: ROBERT L THUNHORST
• 金额: $ 22.05万
• 依托单位: UNIVERSITY OF IOWA
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-12-15 至 2005-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6477077
• 关键词: angiotensins; appetite; atrial natriuretic peptide; blood pressure; homeostasis; hormone regulation /control mechanism; laboratory rat; male; neuroregulation; nutrition related tag; oxytocin; parabrachial nucleus; prosencephalon; rhombencephalon; salt intake; tachykinin; thirst

DESCRIPTION: (Adapted from the Investigator's Abstract) Body fluid balance depends on the gain and loss of water and sodium. Renal mechanisms can slow the rate of water and sodium loss from the body, but ingestion of water and sodium through the mechanisms of thirst and salt appetite is necessary for an ultimate restoration of homeostasis. The maintenance of extracellular volume requires that the central nervous system receives and processes information about the status of body water and sodium. Areas of the forebrain and hindbrain integrate this information in ways that are, on balance, either stimulatory or inhibitory to this ingestive behavior. Several types of vascular sensors and humoral agents normally provide this afferent input. However, under severe environmental challenge or in pathological states, the input and processing of information from sensory systems may be distorted and disrupted. Presently, there is only limited understanding about the nature of interactions of these sensory systems and about how the brain processes this information that is critical for maintaining fluid homeostasis and cardiovascular fitness. The present proposal builds upon the applicant's prior investigations of fluid-related afferent signaling and central processing. The proposed research will employ physiological, pharmacological, and neuroanatomical techniques in the rat that permit the investigation of interactive hormonal (angiotensin, atrial natriuretic peptide), neuropeptidergic (oxytocin, tachykinins) and neural (blood pressure/volume) afferent signals that control hypovolemic thirst and salt appetite. These experiments will generate important new information about basic physiological mechanisms that maintain and restore body fluid homeostasis. An increased understanding of these neurobiological processes will contribute to the well-being of normal individuals exposed to physiological (exercise) and environmental (heat) challenges and of certain types of patients with pathological conditions related to fluid balance (hypertension; congestive heart failure).

描述：（改编自研究者摘要）体液平衡 取决于水和钠的得失。肾脏机制可以减缓 水和钠从体内流失的速度，但摄入的水和钠 通过口渴和盐的机制，食欲是最终的必要条件。 恢复体内平衡。细胞外容积的维持需要 中枢神经系统接收并处理有关 身体水和钠的状态。前脑和后脑的区域整合 这种信息的方式，总的来说，要么是刺激的，要么是抑制的， 这种摄食行为。几种类型的血管传感器和体液 代理通常提供这种传入输入。然而，在严重 环境挑战或在病理状态下，输入和处理 来自感觉系统的信息可能被扭曲和破坏。目前， 对这些相互作用的性质只有有限的了解， 以及大脑如何处理这些信息， 对维持体液平衡和心血管健康至关重要。的 目前的建议是建立在申请人先前的调查基础上的， 液体相关的传入信号和中央处理。拟议研究 将采用生理学、药理学和神经解剖学技术， 允许研究相互作用激素（血管紧张素， 心房钠尿肽），神经肽能（催产素，速激肽）和 控制低血容量性口渴的神经（血压/容量）传入信号 盐的食欲。这些实验将产生重要的新信息 关于维持和恢复体液的基本生理机制 体内平衡对这些神经生物学过程的进一步了解将有助于 有助于健康的正常人暴露于生理 （运动）和环境（热）挑战以及某些类型的患者 与体液平衡相关的病理状况（高血压;充血性 心力衰竭）。