THE EFFECTS OF COMPENSATED CARDIAC-HYPERTROPHY ON DIHYDROPYRIDINE ANDRYANODINE RECEPTORS IN RAT, FERRET AND GUINEA-PIG HEARTS

The number of dihydropyridine and ryanodine receptors (DHP-R and RyR) has been measured in control and hypertrophied ventricles from rats, g uinea pigs and ferrets to determine whether these two channels contrib ute to the alterations in excitation-contraction coupling (ECC), and i n Ca2+ transient during compensated cardiac hypertrophy. We found that ventricular hypertrophy did not change the density of DHP-R, Mild hyp ertrophy did not alter the density of RyR in the rat but decreased it in the guinea-pig and in the ferret (30% and 36%, respectively). Sever e hypertrophy decreased the density of RyR by 20% in the rat and by 34 % in the guinea-pig. Therefore, the decrease is greater in ferret and guinea-pig hearts than in rat heart. We conclude that the sarcoplasmic reticulum (SR) Ca2+ release channels but not the L-type Ca2+ channels could contribute to the slowing of intracellular Ca2+ movements and t o the reduced velocity of shortening of the hypertrophied hearts. We s uggest that, in the guinea pig and ferret hearts which express only th e beta myosin heavy chain (MHC) isoform, the reduced velocity of short ening during hypertrophy is related to the decrease in RyR density, wh ereas in the rat, it is regulated primarily via a shift in the MHC iso form, except in severe hypertrophy in which the moderate decrease in R yR would also be involved.