ROS and NO interaction in the PVN during hypertension?

高血压期间 PVN 中 ROS 和 NO 相互作用？

• 批准号: 7057176
• 负责人: CARRIE A NORTHCOTT
• 金额: $ 2.44万
• 依托单位: MICHIGAN STATE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-06-01 至 2006-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7057176
• 关键词: NAD(P)H dehydrogenase; angiotensin II; biological signal transduction; blood pressure; enzyme activity; free radical oxygen; gamma aminobutyrate; glutamates; hydrogen peroxide; laboratory rat; microinjections; neurochemistry; neuroendocrine system; neurotransmitter transport; nitric oxide; paraventricular nucleus; pathologic process; postdoctoral investigator; renal hypertension; superoxide dismutase; superoxides; telemetry

DESCRIPTION (provided by applicant): The goal of the proposed research is to use an integrative approach to examine the signaling changes, specifically the interrelationships between NO and ROS, that mediate and may influence neurotransmitter activity in renal wrap hypertension. To achieve this goal, three specific hypotheses will be addressed: Hypothesis #1: NAD(P)H oxidase is present and the activity of the enzyme is increased by Ang II and glutamate in the PVN, thus resulting in a" increase of superoxide (O2-) in renal wrap hypertension; Hypothesis #2: Superoxide dismutase (SOD) is present and its activity is decreased contributing to the increase in O2- and a reduction in hydrogen peroxide (H2O2) in the PVN in renal wrap hypertension; and Hypothesis #3: In renal wrap hypertension, there is elevated O2- which combines with NO, reducing NO and ultimately decreasing the inhibitory neurotransmitter GABA; the reduced GABA in the PVN contributes to the rise in arterial pressure. Identifying the changes in these signaling pathways and how they interact to elicit changes in blood pressure would be significantly important for understanding the impact that these pathways have on neurotransmitter activity and hypertension.

描述（由申请人提供）：拟议研究的目标是使用一种综合方法来检查信号变化，特别是NO和ROS之间的相互关系，这些变化介导并可能影响肾包膜高血压中的神经递质活性。为了实现这一目标，将解决三个具体的假设：假设#1：NAD（P）H氧化酶存在，并且该酶的活性通过PVN中的Ang II和谷氨酸盐增加，从而导致”肾包膜高血压中超氧化物（O2-）增加“;假设#2：超氧化物歧化酶（SOD）存在，其活性降低，有助于肾包膜高血压PVN中O2-的增加和过氧化氢（H2 O2）的减少;假设#3：在肾包膜高血压中，存在升高的O2-，其与NO结合，减少NO并最终减少抑制性神经递质GABA; PVN中减少的GABA有助于动脉压的升高。确定这些信号通路的变化以及它们如何相互作用以引起血压的变化对于理解这些通路对神经递质活性和高血压的影响至关重要。