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.