Key Points
- To determine whether functional calcium channel-gated sarcoplasmic reticulum stores mediate calcium signaling and contraction in neonatal and young pediatric human atrial myocytes.
- Isolated atrial myocytes from tissue appendages of pediatric patients aged 3 days to 4 years.
- Assessed calcium currents and intracellular calcium transients using whole-cell patch clamping and fura-2 fluorescence under baseline conditions and following ryanodine or caffeine application.
- Activation of calcium current (2.47 ± 0.23 pA/pF at 0 mV) elicited intracellular calcium transients of 240 ± 45 nM exhibiting a bell-shaped voltage dependence matching the current.
- Intracellular calcium transients were abolished by ryanodine or caffeine, verifying their origin from sarcoplasmic reticulum calcium stores.
- Normalized rates of calcium release increased with donor age, demonstrating progressive developmental increases in calcium signaling efficiency.
Structured PICO
PPopulationIsolated human atrial myocytes obtained from samples of human atrial appendages of 3-day to 4-yr-old patients
IInterventionWhole cell-clamped electrophysiological examination (activation of Ca2+ current)
OOutcomeCharacteristics of Ca2+ signaling (intracellular Ca2+ transients and Ca2+ current)surrogate
This study demonstrates that ICa-gated release of Ca2+ from the sarcoplasmic reticulum is the primary mechanism regulating contraction signaling in early postnatal human atrial myocytes.