Aldosterone in angiotensin II-induced hypertension

描述(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)输注可引起高血压，增加醛固酮(ALDO)，从而增加Na+和水分滞留，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组分应能减轻Ang II诱导的高血压。然而，Aldo在Ang II高血压期间肾脏Na+和水处理中的作用仍不确定。本研究将验证Aldo受体阻断可降低Ang II诱导的高血压患者的Na+和水分滞留，并减轻血压的假说。具体地说，目的是1)确定在安慰剂或盐皮质激素拮抗剂维持治疗的Ang II诱导的高血压大鼠中，Aldo对Na+和水保持的贡献，以及2)确定在Ang II诱导的高血压期间，Aldo对Na+和水保持的贡献，而不依赖于血压的升高和肾脏灌流压的降低。与以前的研究不同，本研究将对Aldo拮抗剂引起的肾脏影响进行更全面的检查。

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.