TY - JOUR
T1 - Contribution of the sodium-calcium exchanger to contractions in immature rabbit ventricular myocytes
AU - Chin, Thomas K.
AU - Christiansen, Gregory A.
AU - Caldwell, Jon G.
AU - Thorburn, Jacqueline
PY - 1997/4
Y1 - 1997/4
N2 - In immature cardiac myocytes, the sarcoplasmic reticulum is sparse. Thus, we hypothesized that sarcolemmal Ca2+ influx through Na+-Ca2+ exchange is the dominant mechanism for modulating intracellular Ca2+ during contractions in fetal and neonatal hearts. We measured Na+ -Ca2+ exchange currents in neonatal and adult rabbit ventricular cells using a rapid solution switch into 0 mM external Na+. The current densities (mean ± SEM) were larger in 8 neonatal cells than in 10 adult cells (5.4 ± 1.38 versus 1.65 ± 0.25 pA/pF). Intracellular Ca2+ transients after inhibiting the sarcoplasmic reticulum with ryanodine and thapsigargin were unchanged in 15 neonatal cells, but decreased in 15 adult cells to 78.9 ± 5.6% of baseline. When the Ca2+ channels were also inhibited by adding nifedipine, Ca2+ transients from Na+-Ca2+ exchange were 30.0 ± 3.5% of baseline in neonatal cells compared with 13.4 ± 3.4% in adult cells. Simultaneous contractions were a larger percent of baseline in neonatal cells (85.7.6 ± 6.4%) than in adult cells (78.9 ± 5.6%) after inhibiting the sarcoplasmic reticulum, and were unmeasurable in many cells from both age groups after inhibiting the Ca2+ channels as well. The ratio of Na+ -Ca2+ exchanger mRNA to sarcoplasmic reticulum Ca2+-ATPase mRNA levels decreased from 1.0) ± 0.13 to 0.4 ± 0.03 to 0.26 ± 0.02 in fetal, neonatal and adult ventricles, respectively. These measurements were consistent with a dominant role for the Na+-Ca2+ exchanger in the immature heart.
AB - In immature cardiac myocytes, the sarcoplasmic reticulum is sparse. Thus, we hypothesized that sarcolemmal Ca2+ influx through Na+-Ca2+ exchange is the dominant mechanism for modulating intracellular Ca2+ during contractions in fetal and neonatal hearts. We measured Na+ -Ca2+ exchange currents in neonatal and adult rabbit ventricular cells using a rapid solution switch into 0 mM external Na+. The current densities (mean ± SEM) were larger in 8 neonatal cells than in 10 adult cells (5.4 ± 1.38 versus 1.65 ± 0.25 pA/pF). Intracellular Ca2+ transients after inhibiting the sarcoplasmic reticulum with ryanodine and thapsigargin were unchanged in 15 neonatal cells, but decreased in 15 adult cells to 78.9 ± 5.6% of baseline. When the Ca2+ channels were also inhibited by adding nifedipine, Ca2+ transients from Na+-Ca2+ exchange were 30.0 ± 3.5% of baseline in neonatal cells compared with 13.4 ± 3.4% in adult cells. Simultaneous contractions were a larger percent of baseline in neonatal cells (85.7.6 ± 6.4%) than in adult cells (78.9 ± 5.6%) after inhibiting the sarcoplasmic reticulum, and were unmeasurable in many cells from both age groups after inhibiting the Ca2+ channels as well. The ratio of Na+ -Ca2+ exchanger mRNA to sarcoplasmic reticulum Ca2+-ATPase mRNA levels decreased from 1.0) ± 0.13 to 0.4 ± 0.03 to 0.26 ± 0.02 in fetal, neonatal and adult ventricles, respectively. These measurements were consistent with a dominant role for the Na+-Ca2+ exchanger in the immature heart.
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U2 - 10.1203/00006450-199704000-00005
DO - 10.1203/00006450-199704000-00005
M3 - Article
C2 - 9098848
AN - SCOPUS:0030934046
SN - 0031-3998
VL - 41
SP - 480
EP - 485
JO - Pediatric Research
JF - Pediatric Research
IS - 4 I
ER -