Henderson Brooke C, Tyagi Suresh C
J Mol Cell Cardiol. 2006 Dec;41(6):959-62. doi: 10.1016/j.yjmcc.2006.09.001. Epub 2006 Oct 13.
Takenaka et al. [Takenaka H, Kihara Y, Iwanaga Y, Onozawa Y, Toyokuni S, Kita T. Angiotensin II, oxidative stress, and extracellular matrix degradation during transition to LV failure in rats with hypertension, J Mol Cell Cardiol, 2006; in press] in this issue have shown that during LV failure in hypertension, there is induction of oxidative stress in which p47 and gp91, and glutathione peroxidase are increased via the NFkB pathway oxidative stress which induces the MMP/TIMP axis, leading to cardiac dilation and failure. The ARB ameliorates the CHF by decreasing oxidative stress [Funabiki K, et al., Combined angiotensin receptor blocker and ACE inhibitor on myocardial fibrosis and LV stiffness in dogs with heart failure, Am J Physiol, 2004; 287(6): H2487-92]. This study supports the notion that the inciting oxidative stress activates the matrix degrading proteinase. That disrupts the connective tissue matrix homeostasis in between the myocyte and endothelial cells causing disruption in synchronization in cardiac systolic contraction and diastolic relaxation. The treatment with ARB mitigates this disruption in cardiac synchrony.
竹中等人（竹中H、木原Y、岩永Y、小野泽Y、丰国S、北T。高血压大鼠左心室衰竭转变过程中的血管紧张素II、氧化应激和细胞外基质降解，《分子与细胞心脏病学杂志》，2006年；即将发表）在本期杂志中表明，在高血压左心室衰竭过程中，会诱导氧化应激，其中p47和gp91以及谷胱甘肽过氧化物酶通过NFkB途径增加，氧化应激会诱导MMP/TIMP轴，导致心脏扩张和衰竭。ARB通过降低氧化应激来改善心力衰竭（船木K等人，联合血管紧张素受体阻滞剂和ACE抑制剂对心力衰竭犬心肌纤维化和左心室僵硬度的影响，《美国生理学杂志》，2004年；287(6):H2487 - 92）。这项研究支持了这样一种观点，即引发的氧化应激会激活基质降解蛋白酶。这会破坏心肌细胞和内皮细胞之间的结缔组织基质稳态，导致心脏收缩期收缩和舒张期舒张同步性破坏。用ARB治疗可减轻心脏同步性的这种破坏。
