心血管反射与慢性心力衰竭课件.pptVIP

Summary 3 PVN中Ang II和AT1受体系统活动增强是导致CHF的CSAR增强的重要机制。 抑制PVN中AT1受体生成能否使CHF大鼠增强的CSAR和RSNA恢复正常？ Intracerebroventricular administration of AT1 receptor mRNA antisense normalized the enhanced CSAR in CHF rats BK 0.04 μg BK 0.4 μg BK 0.04 μg BK 0.4 μg Intracerebroventricular administration of AT1 receptor mRNA antisense decreased RSNA, MAP and HR in CHF rats Microinjection of AT1 receptor mRNA antisense into the PVN inhibited the enhanced CSAR in CHF rats BK 0.04 μg BK 0.4 μg Decreased AT1 receptor mRNA and AT1 receptor protein in the PVN after intracerebroventricular injection of AT1 receptor AS-ODN AT1 receptor mRNA AT1 receptor protein Summary 4 抑制PVN中AT1受体生成使CHF大鼠增强的CSAR和RSNA恢复正常。 PVN中ROS是否调控CSAR？ Microinjection of superoxide anion scavenger, either tempol (20 nmol) or tiron (10 nmol) into the PVN inhibited the CSAR, and superoxide dismutase (SOD) inhibitor diethyldithio-carbamic acid (DETC, 10 nmol) enhanced the CSAR * Superoxide anion scavenger, either tempol or tiron decreased the RSNA and MAP, SOD inhibitor DETC increased the RSNA and MAP Summary 5 清除超氧阴离子抑制CSAR，抑制SOD加强CSAR。 PVN中ROS是否介导Ang II的增强CSAR效应？ Pretreatment with tempol or tiron in the PVN inhibited the augmented CSAR induced by Ang II in the PVN. Pretreatment with DETC had no significant effect on the augmented CSAR induced by Ang II Pretreatment with tempol or tiron in the PVN inhibited the increased RSNA and MAP caused by Ang II in the PVN. Pretreatment with DETC had no significant effect Summary 6 清除超氧阴离子可消除Ang II引起的CSAR增强效应，但抑制SOD不能使Ang II引起的CSAR增强效应进一步显著加强；心室表面应用BK或PVN注射Ang II均引起ROS增多。 表明PVN中ROS调控CSAR，并介导Ang II引起的CSAR增强效应。 PVN中调控CSAR的ROS起源？ NAD(P)H氧化酶？黄嘌呤氧化酶？ Microinjection of NAD(P)H oxidase inhibitor, apocynin (0.1, 1.0 nmol) or phenylarsine oxide (PAO, 1.0 nmol), into the PVN inhibited the CSAR. Xanthine oxidase inhibitor allopurinol (10.0 nmol) had no significant effect on CSAR Pretreatment with microinjection of NAD(P)H oxidase inhibitor, apocynin