课件：ACEI机制之我见南昌.pptx

ACEI机制之我见;;RAAS中血管紧张素Ⅱ和醛固酮 是发挥生物作用的效应分子;ESH/ESC 2013 RASI药物优先适用的情况;应用ACEI之后;Lee et al. Neurohormonal reactivation in heart failure patients on chronic ACE inhibitor therapy: a longitudinal study. European Journal of Heart Failure 1 1999 401]406;;培哚普利显著降低AngII，而ARB升高AngII;ACE2的发现;在病理情况下，ACE/ACE2升高;血管紧张素II和血管紧张素-(1-7)的平衡调节;2016 ESH ;培哚普利增加ACE2活性具有RASS调节作用;Ramipril not augmented cardiac ACE2 expression;;关于醛固酮逃逸;;After an initial suppression/blockade of Ang II/aldosterone, the plasma levels of these 2 compounds often return to normal or even rise above pretreatment levels: the so-called Ang II/aldosterone escape. Given the Ang II/aldosterone escape during RAAS blocker treatment, usually occurring within days-weeks after drug initiation, for many years it was argued that the more blockade, the better, to keep the levels of these active components (or their activity) low. ;不仅是血浆还有组织的ANGII/醛固酮逃逸;Effects of long-term enalapril and losartan therapy of hypertension on cardiovascular aldosterone. Li S1,?Wu P,?Zhong S,?Guo Z,?Lai W,?Zhang Y,?Liang X,?Xiu J,?Li J,?Liu Y. Author information Plasma aldosterone escape is found during long-term angiotensin-converting enzyme inhibitor therapy. Evidence for aldosterone production in cardiovascular tissues raised the question of whether or not aldosterone escape occurs in these tissues. CONCLUSION: This study provides the first evidence that long-term angiotensin-converting enzyme inhibition therapy induces aldosterone escape in hypertensive cardiovascular tissues. Horm Res.?2001;55(6):293-7.; Brugts. JJ. et al. Expert Rev. Cardiovasc. Ther. 2009; 7 (4), 345-360.;培哚普利独特的调节作用;缓激肽通过活化B2受体发挥心血管保护效应;高血压患者缓激肽浓度下降约25%;;培哚普利?8mg重建RAAS-KKS平衡 -抑制AngII、升高缓激肽至正常水平;雅施达8mg显著升高Ang1-7，带来更多的获益;培哚普利8mg重建RAAS-KKS平衡， 确保更卓越心血管保护;Conditional knockout of collecting duct bradykinin B2 receptors exacerbates angiotensin II-induced hypertension during high salt intake;Knockout of Angiotensin 1–7 Receptor Mas Worsens the Course of Two