CONTROL OF SODIUM INTAKE IN THE HINDLIMB UNWEIGHTED RAT

后肢未体重大鼠钠摄入量的控制

• 批准号: 6628586
• 负责人: J Thomas Cunningham
• 金额: $ 4.67万
• 依托单位: UNIVERSITY OF MISSOURI-COLUMBIA
• 依托单位国家: 美国
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-02-01 至 2003-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6628586
• 关键词: baroreceptors; controlled environment chamber; denervation; disease /disorder model; electrolyte balance; gravity; hormone regulation /control mechanism; immobilization of body part; laboratory rat; leg; neuroregulation; nutrition related tag; restricted physical activity; salt intake; saluresis

DESCRIPTION (Verbatim from the application): In the hind limb unweighted (HU) rat model of bed rest and microgravity, HU results in a central movement of body fluid, diuresis and natriuresis, resulting in a decrease in plasma volume. We have observed that rats increase ingestion of saline solution during 24h HU. Further, this ingestion of saline inhibits the decrease in plasma volume normally observed in 24h HU rats. The studies proposed examine the integration of neural and humoral factors influencing sodium ingestion in the HU model of bed rest. The specific aims of the study are: Specific aim 1: Investigate the role of the renal nerves in promoting sodium intake during 24 h HU. Specific aim 2: Investigate the role of hormones in promoting sodium intake during HU. Specific aim 3: Examine the role of the cardiac afferent nerves in regulating the intake of sodium. Specific aim 4: Compare short term (24 h) and long term (14 d) effects of HU on sodium ingestion and plasma volume. We hypothesize that increases in renal afferent nerve activity is critical to HU-induced sodium ingestion. Furthermore, elevated aldosterone may contribute to the ingestion of sodium while stimulation of cardiac afferent nerves may inhibit sodium intake in this model. Integration of these signals by the central nervous system results in a modest sodium intake and maintains plasma volume during HU. During prolonged HU, adaptations may occur which further influence both the ingestion of sodium and blood volume. Understanding bed rest and microgravity-induced changes in body fluid balance requires understanding such factors as the acquisition of solutes. It is hoped that these experiments will contribute to an understanding of both the regulation of body fluid during prolonged bed rest and the problems associated with return to normal posture. Additionally, these data may contribute to understanding of health problems associated with an aging population and with cardiovascular disease such as congestive heart failure.

描述（来自申请的逐字描述）：在未称重的后肢（HU）中 在卧床休息和微重力的大鼠模型中，HU导致 体液、利尿和尿钠排泄，导致血浆容量减少。 我们观察到大鼠在24小时HU期间增加了盐溶液的摄入。 此外，这种盐水的摄入抑制了血浆容量的减少 在24小时HU大鼠中正常观察到。拟议的研究审查了 神经和体液因素影响钠摄入的HU模型， 卧床休息。这项研究的具体目标是： 具体目标1：研究肾神经在促进钠离子代谢中的作用 在24小时HU期间摄入。 具体目标2：研究激素在促进钠摄入中的作用 在胡。 具体目标3：检查心脏传入神经在调节 钠的摄入量。 具体目标4：比较HU对小鼠的短期（24 h）和长期（14 d）影响。 钠摄入量和血浆容量。 我们假设，肾传入神经活动的增加是关键， HU诱导的钠摄入。此外，醛固酮升高可能有助于 与钠的摄入有关，而刺激心脏传入神经可能 抑制该模型中的钠摄入。这些信号的整合， 中枢神经系统导致适度的钠摄入并维持血浆 HU期间的体积。在长时间的HU期间，可能发生适应， 影响钠的摄入和血容量。 了解卧床休息和微重力引起的体液平衡变化 需要了解溶质的获取等因素。希望 这些实验将有助于理解 长期卧床期间体液的调节及相关问题 恢复到正常姿势。此外，这些数据可能有助于 了解与人口老龄化有关的健康问题， 心血管疾病，如充血性心力衰竭。