Sarcolemmal Ca2influx is considered more important for contractions in immature vs mature hearts. To measure developmental changes in the contributions of the Ca2+ channels and 2+-Ca2+ exchanger to contractions, intracellular Ca2transients were measured in field-stimulated ventricular myocytes from 1 -4 day neonatal and 4-6 week adult New Zealand White Rabbits at 24° C. The cells were loaded for 10 minutes with 10 uM indo-1 AM, and washed in normal Tyrode's solution before study. After inhibiting the sarcoplasmic reticulum (SR) with 500 nM thapsigargin and 10 pM ryanodine, Ca2+ transients were unchanged in 22 neonatal cells, but decreased in 20 adult cells to 88.8+3.4% of baseline (mean+SEM, P<0.01). With the SR_and .Ca2+_channejs inhibited (thapsigargin, ryanodine + 20 uM nifedipine), Ca2+ transients from reverse 2+-Ca2+ exchange were larger in 5 neonatal compared to 7 adult cells (61 4+0.7% vs. 11.6+4.9%, P<0 001). With the SRCa2" channels and 2+-Ca2+ exchanger inhibited (thapsigargin, ryanodine + 5 mM Ni2+), Ca2+ transients were eliminated in cells from both age groups. In conclusion, the 2+-Ca2+ exchanger is responsible during contractions for =60% of the rise in intracellular Ca2+ in neonatal vs. = 12% of the rise in adult rabbit myocytes The relative contribution of the Ca2+ channels vs. 2+-Ca2+ exchanger is smaller in the neonatal cells, but 6-fold larger in the adult cells.
|Original language||English (US)|
|State||Published - Dec 1 1996|
All Science Journal Classification (ASJC) codes
- Molecular Biology