CONTROL OF SODIUM INTAKE IN THE HINDLIMB UNWEIGHTED RAT
CONTROL OF SODIUM INTAKE IN THE HINDLIMB UNWEIGHTED RAT
批准号:
6628586
负责人:
J Thomas Cunningham
金额:
$4.67万
依托单位国家:
美国
项目类别:
财政年份:
2001
资助国家:
美国
项目状态:
已结题
起止时间:
2001-02-01 至 2003-06-30
中文摘要
描述(应用程序中的逐字记录):后肢未称重(HU)
卧床休息和微重力的大鼠模型,Hu导致中枢运动
体液、利尿和利钠,导致血浆容量减少。
我们观察到,在24小时内,大鼠对生理盐水的摄入量增加。
此外,这种生理盐水的摄入抑制了血浆体积的减少
通常在HU大鼠24小时内观察。建议的研究检查整合
HU模型中神经和体液因素对钠摄入量的影响
卧床休息。这项研究的具体目的是:
具体目标1:研究肾神经在促钠作用中的作用
24小时内摄取HU。
具体目标2:研究激素在促进钠摄取中的作用
在胡的时候。
具体目标3:检查心脏传入神经在调节中的作用
钠的摄入量。
具体目标4:比较HU的短期(24小时)和长期(14天)效果
钠摄入量和血浆容量。
我们假设肾传入神经活动的增加对
HU诱导的钠摄取。此外,升高的醛固酮可能起到一定作用。
在刺激心脏传入神经的同时摄取钠可能
在这个模型中抑制钠的摄入。这些信号的集成由
中枢神经系统导致适量的钠摄入并维持血浆水平
HU期间的音量。在延长的HU期间,可能会发生进一步的适应
对钠的摄取和血容量都有影响。
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。希望是这样的
这些实验将有助于理解
长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和
心血管疾病,如充血性心力衰竭。
英文摘要
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.
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海外基金