The mammalian heart is known to undergo significant mechanical changes during fetal and neonatal development. The objective of this study was to define the ontogeny of the ryanodine receptor/Ca2+ release channel and SERCA that play the major roles in excitation-contraction coupling. Whole ventricular homogenates of fetal (F) (19 and 22 days in gestation), postnatal (N) (1 and 7 days postnatal), and adult (A) (5 weeks postnatal) Sprague-Dawley rat hearts were used to study [3H]ryanodine binding and oxalate-supported 45Ca2+ uptake. For the ryanodine receptor, the major findings were: (1) The ryanodine receptor density, as determined by maximal [3H]ryanodine binding (Bmax), increased 3 fold between the F22 and A periods (0.26 ± 0.1 vs. 0.73 ± 0.07 pmoles/mg protein, p<0.01), whereas there was no significant change during the F22 and N1 development phases (0.26 ± 0.1 vs. 034 ± 0.01). (2) Affinity of the ryanodine receptor to ryanodine did not significantly change, as suggested by the lack of change in the Kd during the development and maturation. For SERCA, changes started early with an increased rate of Ca2+ uptake in the fetal periods (F19: 8.1 ± 1.1 vs. F22: 193 ± 2.2 nmoles/g protein/min; p<0.05) and peaked by 7 days (N7) of the postnatal age (34.9 ± 2.1). Thus, we conclude that the quantitative changes occur in the ryanodine receptor during myocardial development. Also, the maturation of the Ca2+ uptake appears to start earlier than that of the Ca2+ release.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Biochemistry and Molecular Biology|
|State||Published - Nov 30 2001|
All Science Journal Classification (ASJC) codes
- Molecular Biology