ATRIAL NATRIURETIC PEPTIDE AND ALDOSTERONE SECRETION
心房钠尿肽和醛固酮分泌
基本信息
- 批准号:2218329
- 负责人:
- 金额:$ 21.33万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1987
- 资助国家:美国
- 起止时间:1987-07-01 至 1996-06-30
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Atrial natriuretic peptide (ANP), a potent diuretic and natriuretic
hormone, has receptors throughout the body, including the central nervous
system, the kidney, smooth muscle and the adrenal cortex. An understanding
of the mechanism of action of this peptide will provide insight into the
major counter-regulatory effectors determining volume and blood pressure
homeostasis in humans. This study focuses on elucidating the mechanism of
action of ANP in the adrenal glomerulosa where it inhibits the synthesis
and secretion of aldosterone. This inhibitory action itself has important
physiological implications since aldosterone is the major regulator of salt
and water reabsorption in the kidney, and derangements in its secretion
have been associated clinically with high blood pressure and edematous
states such as congestive heart failure and liver cirrhosis. Occupation of
the ANP receptor(s) induces an increase in cGMP via a unique guanylate
cyclase-containing receptor and a decrease in cAMP via a receptor/G-protein
interaction. In the glomerulosa cell the targets of these second
messengers remain unknown, although the differential modulation of voltage-
dependent Ca2+ channels by ANP and their critical importance to the
maintenance of steroidogenesis indicate that Ca2+ channels may be sites of
regulation. The specific aims of this project are to determine: the
mechanism by which ANP modulates Ca2+ channels, the association of other
Ca2+-dependent protein kinases, and the relationship of cGMP and membrane
potential to the ANP-induced inhibition of steroidogenesis. These studies
will involve patch-clamp analysis of voltage-gated channels,
electrophysiological and spectrofluorometric determinations of membrane
potential, the use of kinase activation assays and Western blotting
techniques, and radioimmunoassays for cyclic nucleotides and aldosterone.
As a result this project will elucidate the mechanism(s) by which ANP
alters the generation of the Ca2+ influx signal and its reception by Ca2+-
dependent effectors and will contribute to our understanding of hypo- nad
hypervolemic states.
心房利钠肽(ANP),一种有效的利尿剂和利钠剂
激素,在全身都有受体,包括中枢神经系统
系统、肾脏、平滑肌和肾上腺皮质。 的理解
这种肽的作用机制将提供深入了解
决定容量和血压的主要反调节效应物
人体内的稳态 本研究的重点是阐明
ANP在肾上腺小球中的作用,在那里它抑制合成
和醛固酮的分泌。 这种抑制作用本身具有重要的
由于醛固酮是盐的主要调节剂,
肾脏的水重吸收和分泌紊乱
在临床上与高血压和水肿有关
如充血性心力衰竭和肝硬化。 占领
ANP受体通过独特的鸟苷酸诱导cGMP增加
含环化酶受体和cAMP通过受体/G蛋白减少
互动 在肾小球细胞中,这些第二个靶点
信使仍然未知,虽然电压的差分调制-
ANP依赖的Ca 2+通道及其对
类固醇生成的维持表明,Ca 2+通道可能是
调控 该项目的具体目标是确定:
ANP调节Ca 2+通道的机制,
Ca 2+依赖性蛋白激酶,cGMP与膜的关系
潜在的ANP诱导的类固醇生成抑制。 这些研究
将涉及电压门控通道的膜片钳分析,
膜的电生理学和荧光分光光度测定
潜在的,使用激酶激活试验和蛋白质印迹法
技术和放射免疫测定环核苷酸和醛固酮。
因此,本项目将阐明ANP
改变Ca 2+内流信号的产生及其被Ca 2 +-
并将有助于我们对hypo-nad的理解
高血容量状态
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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PAULA Q BARRETT其他文献
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{{ truncateString('PAULA Q BARRETT', 18)}}的其他基金
Two-pore domain potassium channels and aldosterone secretion
双孔域钾通道与醛固酮分泌
- 批准号:
8629854 - 财政年份:2008
- 资助金额:
$ 21.33万 - 项目类别:
Two-pore domain potassium channels and aldosterone secretion
双孔域钾通道与醛固酮分泌
- 批准号:
8786092 - 财政年份:2008
- 资助金额:
$ 21.33万 - 项目类别:
Two-pore domain potassium channels and aldosterone secretion
双孔域钾通道与醛固酮分泌
- 批准号:
9187035 - 财政年份:2008
- 资助金额:
$ 21.33万 - 项目类别:
Two-Pore Domain Potassium Channels and Aldosterone Secretion
双孔域钾通道和醛固酮分泌
- 批准号:
7806371 - 财政年份:2008
- 资助金额:
$ 21.33万 - 项目类别:
Two-Pore Domain Potassium Channels and Aldosterone Secretion
双孔域钾通道和醛固酮分泌
- 批准号:
7464697 - 财政年份:2008
- 资助金额:
$ 21.33万 - 项目类别:
Two-Pore Domain Potassium Channels and Aldosterone Secretion
双孔域钾通道和醛固酮分泌
- 批准号:
8054186 - 财政年份:2008
- 资助金额:
$ 21.33万 - 项目类别:
Two-Pore Domain Potassium Channels and Aldosterone Secretion
双孔域钾通道和醛固酮分泌
- 批准号:
7599669 - 财政年份:2008
- 资助金额:
$ 21.33万 - 项目类别:
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