Hypertrophic cardiomyopathy occurs in up to 50% of infants of diabetic mothers (IDMS). Heart defects along with other congenital malformations have been frequently observed from IDMS as well. Since the voltage-dependent Ca++ channels plays very important functions in varies cardiopathological conditions, including arrhythmias and hypertrophy, we are interested in studying the regulation of voltage-dependent Ca++ channels in cardiac myocytes from IDMS.
We have recorded current densities of both T-type and L-type voltage-dependent Ca++ channels in neonatal rat primary cultured myocytes under high (30 mM) and normal (5 mM) glucose conditions. When compared to the normal condition, 24 hours treatment with high glucose resulted in a significant increase in the T-type calcium current density, and a large shift (25 mV toward the negative membrane potential) of the current-voltage relationship (I/V) of the channel. However, the same treatment reduced the L-type calcium current density without a change in its I/V. We have also used fluorescent dye (Flow-3) measurements to demonstrate that chronic treatment of the neonatal myocytes with 30 mM glucose resulted in an increase in the calcium concentration during the relaxation phase of the cardiac cycle, this effect was blocked by NiCl2, a specific T-type calcium channel blocker, in a dose-dependent manner.