cardiac kallikrein-kinin system is upregulated in chronic volume overload and mediates an inflammatory induced collagen loss心脏kallikrein-kinin系统调节慢性卷过载和介导炎症诱导胶原蛋白的损失.pdfVIP

Cardiac Kallikrein-Kinin System Is Upregulated in Chronic Volume Overload and Mediates an Inflammatory Induced Collagen Loss 1,2 4 2 2 2 2 Chih-Chang Wei *, Yuanwen Chen , Lindsay C. Powell , Junying Zheng , Ke Shi , Wayne E. Bradley , 2 5 5 1,2,3 Pamela C. Powell , Sarfaraz Ahmad , Carlos M. Ferrario , Louis J. Dell’Italia 1 Birmingham Veteran Affairs Medical Center, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 2 Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 3 Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 4 Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China, 5 Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States of America Abstract Background: The clinical problem of a ‘‘pure volume overload’’ as in isolated mitral or aortic regurgitation currently has no documented medical therapy that attenuates collagen loss and the resultant left ventricular (LV) dilatation and failure. Here, we identify a potential mechanism related to upregulation of the kallikrein-kinin system in the volume overload of aortocaval fistula (ACF) in the rat. Methodology/Principal Findings: LV interstitial fluid (ISF) collection, hemodynamics, and echocardiography were performed in age-matched shams and 4 and 15 wk ACF rats. ACF rats had LV dilatation and