Yonemochi H, Nakagawa M, Iwao T, Ito M
Department of Laboratory Medicine, Medical University of Oita.
Rinsho Byori. 1996 Nov;44(11):1037-42.
It is recognized that heart failure in patients with atherosclerotic lesion is the result of ischemia. However, there may also be cardiac cell dysfunction independent of ischemia, as factors advancing both of atherosclerosis and heart failure are discovered. The renin-angiotensin system is one of factor and angiotensin-converting enzyme inhibitor (ACEi) prevents progression of atherosclerotic lesion and heart failure. To elucidate the association of atherosclerosis and cardiac cell dysfunction, we investigated the effects of ACEi on cultured cardiac myocytes. Captopril increased beta-receptor density of myocytes and augmented the response to isoproterenol. CV-3480, a ACEi, also up-regulated beta-receptors but angiotensin I, angiotensin II and angiotensin type I receptor antagonist did not. Bradykinin B2 receptor blocker, HOE140, suppressed the effect of captopril on cultured cells. The results suggest that ACEi up-regulated beta-receptors and augmented the response to beta-receptor agonist through BK potentiation.
人们认识到,患有动脉粥样硬化病变的患者发生心力衰竭是缺血的结果。然而,也可能存在与缺血无关的心肌细胞功能障碍,因为发现了促进动脉粥样硬化和心力衰竭的因素。肾素-血管紧张素系统就是其中一个因素,血管紧张素转换酶抑制剂(ACEi)可防止动脉粥样硬化病变和心力衰竭的进展。为了阐明动脉粥样硬化与心肌细胞功能障碍之间的关联,我们研究了ACEi对培养心肌细胞的影响。卡托普利增加了心肌细胞的β受体密度,并增强了对异丙肾上腺素的反应。一种ACEi,CV-3480,也上调了β受体,但血管紧张素I、血管紧张素II和血管紧张素I型受体拮抗剂则没有。缓激肽B2受体阻滞剂HOE140抑制了卡托普利对培养细胞的作用。结果表明,ACEi通过增强缓激肽上调β受体并增强对β受体激动剂的反应。