Aldosterone in angiotensin II-induced hypertension

醛固酮在血管紧张素II诱导的高血压中的作用

• 批准号: 6883173
• 负责人: Rudy M Ortiz
• 金额: $ 4.99万
• 依托单位: UNIVERSITY OF CALIFORNIA, MERCED
• 依托单位国家: 美国
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-04-01 至 2006-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6883173
• 关键词: angiotensin /renin /aldosterone hypertension; angiotensin II; angiotensin receptor; edema; enzyme linked immunosorbent assay; excretion; flame photometry; hemodynamics; kidney circulation; kidney disorder; laboratory rat; light microscopy; microcirculation; postdoctoral investigator; radioimmunoassay; renin angiotensin system; saluresis; sodium ion; spectrometry; statistics /biometry; telemetry

DESCRIPTION (provided by applicant): The renin-angiotensin-aldosterone system (RAAS) regulates Na+ balance and blood pressure. Angiotensin II (Ang II) infusion induces hypertension and increases aldosterone (aldo), which should increase Na+ and water retention and exacerbate the hypertension. Elevated aldo has also been associated with fibrosis and tissue damage. Therefore, blockade of RAAS components should attenuate Ang II-induced hypertension. However, the contribution of aldo in renal Na+ and water handling during Ang II hypertension remains inconclusive. This study will test the hypothesis that aldo receptor blockade decreases Na+ and water retention and attenuates blood pressure in Ang II-induced hypertension. Specifically, the aims are 1) to determine the contribution of aldo to Na+ and water retention in Ang II-induced hypertensive rats treated with placebo or mineralocorticoid antagonists maintained, and 2) to determine the contribution of aldo to Na+ and water retention during Ang II-induced hypertension independent of elevated blood pressure and in the presence of reduced renal perfusion pressure. Unlike previous studies, the present study will provide a more comprehensive examination of the renal effects induced by aldo antagonism.

描述（由申请人提供）：肾素-血管紧张素-醛固酮系统（RAAS）调节Na+平衡和血压。血管紧张素II（Ang II）输注诱导高血压并增加醛固酮（aldosterone，aldo），这将增加Na+和水潴留并加重高血压。aldo升高也与纤维化和组织损伤有关。因此，阻断RAAS组分应减弱Ang II诱导的高血压。然而，在血管紧张素II高血压过程中，醛在肾脏Na+和水处理中的作用仍然没有定论。本研究将验证Aldo受体阻断剂降低Ang II诱导的高血压中Na+和水潴留并降低血压的假设。具体而言，目的是1）确定在用安慰剂或盐皮质激素拮抗剂治疗的Ang II诱导的高血压大鼠中，醛对Na+和水潴留的贡献，以及2）确定在Ang II诱导的高血压期间，醛对Na+和水潴留的贡献，其独立于血压升高和存在肾灌注压降低。与以前的研究不同，本研究将提供一个更全面的检查由aldo拮抗作用引起的肾脏影响。