1. Myocardial hypertrophy is a common pathologicalchange that accompanies cardiovascular disease. Dopamine D2receptors have been demonstrated in cardiovascular tissues.However, the pathophysiological involvement of D2 receptorsin myocardial hypertrophy is unclear. Therefore, the effects ofthe D2 receptor agonist bromocriptine and the D2 receptorantagonist haloperidol on angiotensin (Ang) II-or endothelin(ET)-1-induced hypertrophy of cultured neonatal rat ventricularmyocytes were investigated in the present study.2. Protein content and protein synthesis, determined byexamining [3H]-leucine uptake, were used as estimates of cardiomyocytehypertrophy. The expression of D2 receptor proteinin neonatal rat ventricular myocytes was determined usingwestern blotting. Changes in [Ca2?]i in cardiomyocytes wereobserved by laser scanning confocal microscopy.3. Angiotensin II and ET-1, both at 10 nmol/L, inducedmyocyte hypertrophy, as demonstrated by increased proteincontent and synthesis, [Ca2?]i levels, protein kinase C (PKC)activity and phosphorylation of extracellular signal-regulatedkinase, c-Jun N-terminal kinase and mitogen-activated proteinkinase (MAPK) p38 (p38). Concomitant treatment of cells with10 nmol/L AngII plus 10mol/L bromocriptine significantlyinhibited cardiomyocyte hypertrophy, MAPK phosphorylationand PKC activity in the membrane, as well as [Ca2?]i signallingpathways, compared with the effects of AngII alone. In addition, 10 mol/L bromocriptine significantly inhibited cardiomyocytehypertrophy induced by 10 nmol/L ET-1. However, pretreatmentwith haloperidol (10mol/L) had no significant effects oncardiomyocyte hypertrophy induced by either AngII or ET-1.4. In conclusion, D2 receptor stimulation inhibits AngIIinducedhypertrophy of cultured neonatal rat ventricularmyocytes via inhibition of MAPK, PKC and [Ca2?]i signallingpathways.