RENAL SODIUM TRANSPORTERS IN CONTROL OF ARTERIAL BLOOD PRESSURE
肾钠转运蛋白控制动脉血压
基本信息
- 批准号:6202277
- 负责人:
- 金额:$ 20.67万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1999
- 资助国家:美国
- 起止时间:1999-12-01 至 2001-11-30
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Hypertension is a major health problem in the United States that ultimately
affects about one quarter of the population and contributes to heart
attacks, stroke, and kidney failure. Available evidence suggests that a
major mechanism for the regulation of arterial blood pressure resides in
the ability of the kidneys to control extracellular fluid volume by
alterations in the excretion of salt and water. Thus, the transporters
that mediate sodium reabsorption across the apical membranes of renal
epithelial cells, some of which serve as targets for antihypertensive
medications, are likely to serve as integral components of the renal
systems mediating control of arterial blood pressure. To test this
hypothesis we propose to develop and analyze mouse models in which the
genes encoding these transporters are ablated. In aim 1 we will use gene
targeting technology to develop mice with disruptions of the genes encoding
the apical Na/H exchanger of the proximal tubule, the Na,K,2C1cotransporter
of the thick ascending limb of Henle, the NaC1 cotransporter of the distal
convoluted tubule, and the Na channel of the collecting duct. The
viability of mutant offspring will be assessed by analysis of genotype
frequency, embryonic/fetal development, birthweight, survival and growth
rate, and tissue histology, thereby allowing a determination of whether
each transporter is essential for survival or, alternatively, whether there
are compensatory mechanisms that overcome the loss of a particular
transporter. In aim 2 we will determine whether these primary genetic
defects, in which one or both copies of the genes encoding each of the
apical sodium transporters has been disrupted, are capable of producing a
chronic alteration in arterial blood pressure. By utilizing these
genetically altered animals, in which sodium reabsorption in individual
nephron segments has been perturbed, it will be possible to assess the
relative importance of each transporter and nephron segment in the control
of arterial blood pressure, as well as some of the renal compensatory
mechanisms. Wild-type and mutant animals will be maintained on low,
normal, and high sodium diets, and chronic.alterations in blood pressure
will be analyzed by both femoral artery catheterization and tail cuff
procedures. Alterations in glomerular filtration rate, renal plasma flow,
plasma volume, urinary excretion of Na+ and K+, plasma levels of renin and
aldosterone, and Na,K-ATPase activity along the nephron will be assessed,
and morphological correlates of compensatory changes will be analyzed by
electron microscopy. We anticipate that the mice developed in this
proposal will become valuable and widely used models for detailed analysis
of the mechanisms underlying the relationship between renal Na+ handling
and arterial blood pressure.
高血压是美国的一个主要健康问题,最终
项目成果
期刊论文数量(0)
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会议论文数量(0)
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GARY EDWARD SHULL其他文献
GARY EDWARD SHULL的其他文献
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{{ truncateString('GARY EDWARD SHULL', 18)}}的其他基金
Mouse Models for Ion Homeostasis Defects in Heart
心脏离子稳态缺陷的小鼠模型
- 批准号:
7923967 - 财政年份:1999
- 资助金额:
$ 20.67万 - 项目类别:
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