To clarify the molecular basis for changes in
L-type calcium channel (VLCC) density in ventricular
hypertrophy, we analyzed the
mRNA expression of all the subunits including the main subunit alpha1c and auxiliary subunits (alpha2delta, beta2 and beta3) composing VLCC in rat
right ventricular hypertrophy (RVH) induced by
monocrotaline injection. To test the hypothesis that the expression of each subunit might change differently during progression of RVH, leading to an altered electrophysiologic outcome for VLCC, we investigated the ratio of the
mRNA level of each auxiliary subunit to the main subunit. After
monocrotaline injection, alpha1c
mRNA showed a transient decrease on the 14th day and thereafter significantly increased to reach approximately 1.8 fold that of the control level on the 21st day. The auxiliary subunit alpha2delta
mRNA showed a pattern similar to that of alpha1c. The beta3
mRNA increased rapidly after
monocrotaline injection and increased approximately 4.1 fold. On the other hand, beta2
mRNA showed no significant changes. Accordingly, only the
mRNA ratio of beta3 to alpha1c showed a significant increase among the auxiliary subunits after the
monocrotaline injection. The ratio increased to a maximum of approximately 5.7 fold on the 14th day and thereafter decreased. These results suggest that VLCC density may be modified not only by alpha1c but also by its auxiliary subunit expression in ventricular
hypertrophy, and provide a clue for understanding the controversial electrophysiologic results on VLCC density in hypertrophied hearts.