The goal of this study was to characterize the Ca2+-release channel in whole homogenates of left (LV) and right ventricles (RV) of fetal (22 days in gestation) and adult Sprague-Dawley rat hearts using [3H]ryanodine binding and 45Ca2+ fluxes. Although many features of the Ca2+-release channels were similar in fetal and adult hearts, biochemical assays revealed quantitative differences. Similar properties include 1) Ca2+-sensitive cooperative ryanodine binding to Ca2+-release channel, measured as Ca2+ concentration for half-maximal activation (fetal LV: 0.13 ± 0.02 μM; adult LV: 0.15 ± 0.02 μM) and Hill coefficient (fetal LV: 2.5 ± 0.9; adult LV: 2.7 ± 0.5), and 2) caffeine-sensitive ryanodine binding, measured as the percent increase in ryanodine binding induced by caffeine (fetal LV: 148.8 ± 16.9% vs. adult LV: 171.4 ± 34.9%). The distinguishing property was the lower Ca2+-release channel density in the fetal heart (LV: 0.22 ± 0.03 pmol/mg protein) compared with adult heart (LV: 0.59 ± 0.04 pmol/mg protein; P < 0.05), as determined by [3H]ryanodine binding. The lower density of Ca2+-release channel is supported by the finding that there is very low ryanodine-sensitive oxalate-supported 45Ca2+ uptake in the fetal heart. The tested characteristics of the Ca2+-release channel were similar between LV and RV in both fetal and adult rat hearts. Our results indicate that expression of Ca2+-release channels in sarcoplasmic reticulum increases during postnatal growth in the rat heart. This is consistent with previous physiological reports that Ca2+ available for excitation-contraction coupling in the fetal heart is derived mainly from transsarcolemmal Ca2+ influx.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||3 38-3|
|State||Published - Jan 1 1995|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)