Pharmacology of G-Protein-linked Signaling in Cardiac Fibroblasts

The responses of CFs to individual hormones are beginning to be cataloged (Tables II, III and IV). It is not yet known whether CFs from subjects with cardiovascular diseases differ from “normal” CFs. Actions of hormones are likely much more complex in vivo than in vitro, as the example of β-adrenergic agonists makes clear. In addition, cross-talk amongst signaling pathways when cells are stimulated by multiple agonists complicates the picture and the overall responses. Moreover, although elevated cyclic AMP reduces collagen synthesis by CFs in culture, other components of the ECM, such as fibronectin, seem to be derived from genes with cyclic AMP response elements (CREs). Despite these complexities we believe that activation and blockade of cell surface receptors, especially G-protein linked, could be fruitful way of manipulating CF function in vivo.