Human cardiac fibroblasts and receptors for angiotensin II and bradykinin: a potential role for bradykinin in the modulation of cardiac extracellular matrix.

Evidence derived from in vivo experimental studies performed with angiotensin converting enzyme inhibitors (ACEi) indicates that these agents are capable of modulating the process of cardiac hypertrophy and fibrosis. The antifibrotic actions of ACEi are thought to be derived from their capacity to block the production of angiotensin II and, thus, its action on the cardiac fibroblast. However, in contrast to rat hearts, human myocardium has low levels of angiotensin II receptors. Evidence indicates that enhanced bradykinin (BK) levels result from the action of ACEi. In vivo data derived from the use of the BK blocker HOE140 suggests a role for BK in repressing the process of cardiac hypertrophy and fibrosis. Little is known as to the abundance of angiotensin II and BK receptors in human cardiac fibroblasts. Data presented in this study indicates that in cultured human cardiac fibroblasts there is apparently few angiotensin II receptors whereas as in other species there is evidence for the presence of BK receptors. Further studies need to be performed to establish the potential role that BK plays in modulating human cardiac fibroblast function.