Autoregulatory Impairment in Na-Sensitive hypertension
钠敏感性高血压的自身调节损伤
基本信息
- 批准号:7228245
- 负责人:
- 金额:$ 19.29万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2006
- 资助国家:美国
- 起止时间:2006-05-01 至 2009-04-30
- 项目状态:已结题
- 来源:
- 关键词:adenosine triphosphateangiotensin /renin /aldosterone hypertensionarteriolesbiological signal transductionblood vessel disordercalcium indicatorcalcium ioncytokinefluorescence spectrometryimmunocytochemistryinterleukin 6kidney functionlaboratory mousemicrocirculationneuroregulationpurinergic receptorreceptor sensitivitysomatic afferent nervespontaneous hypertensive rattransforming growth factorsvascular smooth musclevideo microscopywestern blottings
项目摘要
The current proposal will determine the role of P2 receptors in the impaired autoregulatory behavior exhibited by afferent arterioles from salt-sensitive hypertensive animals. Emphasis will focus on the responsiveness of the microvasculature to P2 receptor stimulation by ATP. Previous work from our laboratory has implicated ATP as the messenger molecule released from salt-sensing, macula densa cells to effect autoregulatory adjustments in preglomerular resistance. ATP is also considered to be essential element in the renal response to increased salt. Preliminary data indicate that autoregulatory capability and responsiveness to P2 receptor
activation by ATP is attenuated in afferent arterioles in kidneys from angiotensin II-infused hypertensive rats. These observations support the central hypothesis that P2 receptors mediate autoregulatory adjustments in afferent arteriolar diameter and that P2 receptor activation is impaired in hypertension by the actions of locally generated cytokines. Accordingly, experiments will focus on the regional responsiveness of afferent arterioles from hypertensive and normotensive rats, to P2 receptor stimulation and will assess the impact of specific renal cytokines on these responses. Specific Aim #1 will test the hypothesis that decreased P2
receptor activation mediates impairment of autoregulatory responses in kidneys from salt-sensitive hypertensive animals.. Specific Aim #2 will test the hypothesis that locally generated cytokines impair afferent arteriolar responsiveness P2 receptor activation. These studies will focus on the microvascular responsiveness to P2 receptor activation and the calcium influx pathways utilized by them in the myogenic and TGF-dependent regions of the afferent arteriole. Specific Aim #3 will test the hypothesis that influx-dependent Ca 2+ signaling mechanisms are responsible for impaired autoregulatory responsiveness in animals
developing salt-sensitive hypertension. We will use freshly isolated preglomerular smooth muscle cells from kidneys of normotensive and hypertensive rats fed normal and high salt diets. Calcium signaling pathways invoked by P2 receptor activation will be examined using fura-2. We will assess the impact of chronic infusions of IL-6 or TGF-beta on the calcium influx pathways invoked by P2 receptor stimulation.
目前的建议将确定P2受体在盐敏感高血压动物传入小动脉表现出的自我调节行为受损中的作用。重点将集中在微血管对ATP刺激P2受体的反应性。我们实验室之前的研究表明,ATP是盐感细胞、黄斑致密细胞释放的信使分子,影响肾小球前抵抗的自我调节。ATP也被认为是肾脏对高盐反应的必要元素。初步的数据显示了其对P2受体的自我调节能力和反应性
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)
数据更新时间:{{ journalArticles.updateTime }}
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
Edward W Inscho其他文献
Edward W Inscho的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
{{ truncateString('Edward W Inscho', 18)}}的其他基金
Conference on Control of Renal Function in Health and Disease
健康与疾病中肾功能控制会议
- 批准号:
9756663 - 财政年份:2019
- 资助金额:
$ 19.29万 - 项目类别:
Receptor Specific Mechanisms of Endothelin Control of the Renal Microcirculation
内皮素控制肾微循环的受体特异性机制
- 批准号:
8002583 - 财政年份:2010
- 资助金额:
$ 19.29万 - 项目类别:
The Inflammatory Cytokines, MCP-1 and TGF-Beta, Mediate Renal Autoregulatory Impa
炎症细胞因子 MCP-1 和 TGF-Beta 介导肾脏自动调节影响
- 批准号:
8011355 - 财政年份:2010
- 资助金额:
$ 19.29万 - 项目类别:
The cytokines, MCP-1 and TGF-beta, mediate renal autoregulatory impairment
细胞因子 MCP-1 和 TGF-β 介导肾脏自动调节功能障碍
- 批准号:
8606758 - 财政年份:2010
- 资助金额:
$ 19.29万 - 项目类别:
The cytokines, MCP-1 and TGF-beta, mediate renal autoregulatory impairment
细胞因子 MCP-1 和 TGF-β 介导肾脏自动调节功能障碍
- 批准号:
8900028 - 财政年份:2010
- 资助金额:
$ 19.29万 - 项目类别:
The cytokines, MCP-1 and TGF-beta, mediate renal autoregulatory impairment
细胞因子 MCP-1 和 TGF-β 介导肾脏自动调节功能障碍
- 批准号:
8208158 - 财政年份:2010
- 资助金额:
$ 19.29万 - 项目类别:
The Inflammatory Cytokines, MCP-1 and TGF-Beta, Mediate Renal Autoregulatory Impa
炎症细胞因子 MCP-1 和 TGF-Beta 介导肾脏自动调节影响
- 批准号:
7753439 - 财政年份:2010
- 资助金额:
$ 19.29万 - 项目类别:
The cytokines, MCP-1 and TGF-beta, mediate renal autoregulatory impairment
细胞因子 MCP-1 和 TGF-β 介导肾脏自动调节功能障碍
- 批准号:
8403967 - 财政年份:2010
- 资助金额:
$ 19.29万 - 项目类别:
Autoregulatory Impairment in Salt-Sensitive Hypertension
盐敏感性高血压的自身调节损伤
- 批准号:
7433777 - 财政年份:2007
- 资助金额:
$ 19.29万 - 项目类别:
Autoregulatory Impairment in Na-Sensitive hypertension
钠敏感性高血压的自身调节损伤
- 批准号:
7063184 - 财政年份:2005
- 资助金额:
$ 19.29万 - 项目类别: