title: Catecholamines in cardiac hypertrophy.
abstract: There has been intense interest in the roles catecholamines may play in compensatory myocardial hypertrophy. This article reviews the following: (1) chronic infusions of catecholamines in experimental animals result in cardiac 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 that mechanical activity is sufficient to cause increased protein synthesis and cell growth; (3) in neonatal myocyte cell cultures, alpha-adrenergic agonists are powerful stimulants for protein synthesis and cell growth. Beta-adrenergic stimulation of nonmyocyte myocardial cells causes release of a factor that promotes protein synthesis in neonatal myocytes. Either alpha or beta stimulation, probably through different mechanisms, appears to have growth-promoting effects on isolated adult myocytes in culture; (4) alpha stimulation is transduced through the Gq pathway and its activation of phospholipase C, cleavage of phosphatidylinositol (4,5)-bisphosphate, and then further through the ras/raf, mitogen-activated protein (MAP) kinase system; (5) transgenic mice with upregulation of catecholamine-related systems have not clarified the independent role of either the alpha- or beta-adrenergic pathway; and (6) observations in humans suggest that mechanical factors predominate in the development and regression of cardiac hypertrophy. Humoral mechanisms, 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.
authors.affiliation: Albert Einstein College of Medicine, Department of Medicine, Bronx, New York 10461, USA.
authors.forename: J
authors.initials: J
authors.lastname: Scheuer
mesh_terms: D000322:Adrenergic Agonists / Q000494:pharmacology; D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002395:Catecholamines / Q000378:metabolism / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D011941:Receptors, Adrenergic / Q000187:drug effects / Q000378:metabolism
chemical_list: D000322:Adrenergic Agonists; D002395:Catecholamines; D011941:Receptors, Adrenergic