Gq signaling in cardiac adaptation and maladaptation

Accumulating evidence suggests that cardiac responses to a number of circul ating or locally released humoral factors contribute to adaptive responses after hemodynamic stress or myocardial injury. lit particular hormones such as angiotensin II, endothelin I, norepinephrine and prostaglandin F-2 alph a which bind to and activate cardiomyocyte membrane receptors coupled to th e Gq class of GTP binding proteins have been implicated in the development and ultimate decompensation of cardiac hypertrophy. Herein we summarize rec ent developments in cultured cardiomyocyte and transgenic mouse systems whi ch are defining the phenotypes resulting front Gq signaling events in cardi omyocytes, and which are elucidating the critical downstream mediators. Pos tulated robs for protein kinase C, p38 MAP kinase and jun-N terminal kinase are discussed in relation to Gq-mediated cardiomyocyte hypertrophy and apo ptotic signaling. The evidence to date suggests that molecular targeting of Gq or its effecters has the potential to modify cardiac adaptive and malad aptive responses to stress or injury. (C) 1999, Elsevier Science Inc.