Evidence for presence of Ca2+ channel-gated Ca2+ stores in neonatal human atrial myocytes.

The characteristics of Ca2+ signaling in fura 2-loaded whole cell-clamped myocytes obtained from samples of human atrial appendages of 3-day to 4-yr-old patients were examined. In isolated myocytes, activation of Ca2+ current (ICa) (2.47 +/- 0.23 pA/pF) at 0 mV elicited sizable intracellular Ca2+ (Cai) transients (240 +/- 45 nM), which were caused by the release of Ca2+ from intracellular stores as they were suppressed in the presence of ryanodine or caffeine. The voltage dependence of both Cai transients and ICa were similar and bell shaped. The rate of release of Ca2+, normalized for the maximal Ca2+ release, increased with age, indicating increased efficiency of Ca2+ signaling in more mature myocytes. The results suggest that ICa-gated release of Ca2+ from the sarcoplasmic reticulum is the primary mechanism regulating the signaling of contraction in early postnatal as well as older human atrial myocytes.