Cardiac myocytes respond to biomechanical stress by initiating cellular pro
cesses that lead to hypertrophy. Although cardiac hypertrophy is a response
to increased stress on the heart, it is associated with elevated plasma ca
techolamine levels and an increase in cardiac morbidity and mortality. Unde
rstanding the cellular signals that initiate the hypertrophic response will
be of critical importance to identify pathways that mediate the maladaptiv
e deterioration of the hypertrophic heart to one of cardiac failure. This r
eview will focus on the role of G protein-coupled receptors in the activati
on of signalling pathways in the heart, such as the mitogen activated prote
in kinase and phosphoinositide-3 kinase pathways.