Catecholamines in cardiac hypertrophy

There has been intense interest in the roles catecholamines may play in com pensatory myocardial hypertrophy. This article reviews the following: (1) c hronic infusions of catecholamines in experimental animals result in cardia c hypertrophy, but in many of the studies mechanical factors have played a role; (2) experiments using isolated papillary muscles and isolated hearts, stretched isolated myocytes, and denervated hearts in vivo demonstrate tha t mechanical activity is sufficient to cause increased protein synthesis an d cell growth; (3) in neonatal myocyte cell cultures, alpha-adrenergic agon ists are powerful stimulants for protein synthesis and cell growth. Beta-ad renergic stimulation of nonmyocyte myocardial cells causes release of a fac tor that promotes protein synthesis in neonatal myocytes, Either alpha or b eta stimulation, probably through different mechanisms, appears to have gro wth-promoting effects on isolated adult myocytes in culture; (4) alpha stim ulation is transduced through the Gq pathway and its activation of phosphol ipose C, cleavage of phosphatidylinositol (4,5)-bisphosphate, and then furt her through the ras/raf, mitogen-activated protein (MAP) kinase system; (5) transgenic mice with upregulation of catecholamine-related systems have no t clarified the independent role of either the alpha- or beta-adrenergic pa thway; and (6) observations in humans suggest that mechanical factors predo minate in the development and regression of cardiac hypertrophy. Humoral me chanisms, including catecholamines, may play a role, but their quantitative importance has not been determined. It is hypothesized that catecholamines may play a role in transition from the adaptive to the maladaptive state. (C)1999 by Excerpta Medica, Inc.