Superoxide and TP-Rs in Salt Sensitive Hypertension

盐敏感性高血压中的超氧化物和 TP-R

• 批准号: 6829236
• 负责人: JAN M WILLIAMS
• 金额: $ 2.7万
• 依托单位: AUGUSTA UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-08-15 至 2006-08-14
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6829236
• 关键词: angiotensin /renin /aldosterone hypertension; catalase; endothelin; hemodynamics; hormone receptor; immunologic assay /test; kidney circulation; laboratory rat; predoctoral investigator; radioimmunoassay; receptor expression; renal failure; superoxides; telemetry; thromboxanes; ultrasound blood flow measurement; urinalysis

DESCRIPTION (provided by applicant): Blocking ETB receptors causes salt-sensitive hypertension and an increase in ET-1 plasma and urine levels. ET-1 also has been demonstrated to stimulate superoxide and to promote TxA2 synthesis through the ETA receptor. Blockade of the ETA receptor will prevent the hypertension produced by chronic ETB blockade, but the mechanism is not completely understood. The overall hypothesis is superoxide and thromboxane contributes to the pathophysiological effects of ETB receptor blockade in rats on a high salt diet. Specific Aims: 1. To test the hypothesis that superoxide contributes to the hypertension produced by ETB receptor blockade. 2. To test the hypothesis that TP receptor activation contributes to the hypertension produced by ETB receptor blockade. 3. To test the hypothesis that cortical blood flow and medullary blood flow is decreased in rats treated with an ETB receptor antagonist along with ET-1 infusion through the stimulation of TxA2 and superoxide acutely.

描述（由申请人提供）：阻断ETB受体可导致盐敏感性高血压以及血浆和尿液ET-1水平升高。ET-1还被证明通过ETA受体刺激超氧化物和促进TxA 2合成。阻断ETA受体可预防慢性ETB阻断引起的高血压，但其机制尚不完全清楚。总体假设是超氧化物和血栓素有助于高盐饮食大鼠中ETB受体阻滞的病理生理效应。 具体目标： 1.验证超氧阴离子参与阻断ETB受体引起的高血压的假说。2.验证TP受体激活与ETB受体阻断剂引起的高血压有关的假设。3.为了验证以下假设：在用ETB受体拮抗剂沿着ET-1输注处理的大鼠中，通过急性刺激TxA 2和超氧化物，皮质血流量和髓质血流量减少。