Creatine phosphokinase-mediated transport of energy from the site of produc
tion to the site of consumption is a key process for meeting the energy-dem
ands of reactions in cytosol. The mitochondrial creatine phosphokinase (mCP
K) plays an important role in this process, with the enzyme activity locali
zed particularly in the mitochondrial contact sites (MiCS). Earlier studies
in adult animals have shown that the formation of MiCS varies in response
to the energy demand and the physiological state of the heart, and it is st
imulated by an increase in [Ca2+](i). However, there is little known about
MiCS formation in juvenile hearts, characterized by metabolism different fr
om adult hearts. In the present study we investigated the modulation of MiC
S formation via Ca2+ in hearts of 14-day-old rats. The moderate response of
MiCS to various stimuli (elevated extracellular Ca2+, diltiazem, cardiac a
rrest by Cd2+) may refer to a still increased intracellular Ca2+ concentrat
ion, the incomplete development of mitochondrial energy production as well
as to persistingly high energy demand of the developing heart.