The structural and functional integrity of the heart can be attributed to an ex racellular matrix (ECM) composed mainly of fibrillar collagens (types I and III). Remodeling of the collagen matrix is implicit in cardiac fibrosis and this event may contribute to the development of congestive heart failure (CHF) due to idiopathic cardiomyopathy (CMP). Cardiac fibrillar collagen turnover is known to be achieved by a balance between collagen synthesis and removal, and both of these processes are attributed to cardiac fibroblasts. It is possible that an imbalance in collagen turnover resulting in changes in patterns of collagen deposition and removal attends overt cardiac fibrosis in cardiomyopathic hearts. Thus we tested the hypothesis that cardiac matrix metalloproteinases (MMP-1, MMP-2 and MMP-9) are activated in an experimental model of CMP (UM-X7.1 strain of Syrian cardiomyopathic hamsters) via an angiotensin II type I (AT$\sb1$) receptor dependent pathway. (Abstract shortened by UMI.)