Cardiogenesis depends on a tightly regulated balance between proliferation and 
differentiation of cardiac progenitor cells (CPCs) and their cardiomyocyte 
descendants. While exposure of early mouse embryos to Ca(2+) channel antagonists 
has been associated with abnormal cardiac morphogenesis, less is known about the 
consequences of Ca(2+) channel blockade on proliferation and differentiation of 
CPCs at the cellular level. Here we showed that at embryonic day (E) 11.5, the 
murine ventricles express several L-type and T-type Ca(2+) channel isoforms, and 
that the dihydropyridine Ca(2+) channel antagonist, nifedipine, blunts 
isoproterenol induced increases in intracellular Ca(2+). Nifedipine mediated 
Ca(2+) channel blockade was associated with a reduction in cell cycle activity 
of E11.5 CPCs and impaired assembly of the cardiomyocyte contractile apparatus. 
Furthermore, in cell transplantation experiments, systemic administration of 
nifedipine to adult mice receiving transplanted E11.5 ventricular cells 
(containing CPCs and cardiomyocytes) was associated with smaller graft sizes 
compared to vehicle treated control animals. These data suggest that 
intracellular Ca(2+) is a critical regulator of the balance between CPC 
proliferation and differentiation and demonstrate that interactions between 
pharmacological drugs and transplanted cells could have a significant impact on 
the effectiveness of cell based therapies for myocardial repair.