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Biophysical Journal 86:966-977 (2004)
© 2004 The Biophysical Society

Calcium Buffering and Excitation-Contraction Coupling in Developing Avian Myocardium

Tony L. Creazzo *, Jarrett Burch * and Robert E. Godt {dagger}

* Neonatal/Perinatal Research Institute, Department of Pediatrics/Neonatology Division, Duke University Medical Center, Durham, North Carolina; and {dagger} Department of Physiology, Medical College of Georgia, Augusta, Georgia

Correspondence: Address reprint requests to Tony L. Creazzo, PhD, Neonatal/Perinatal Research Institute, Pediatrics/Neonatology Division, Duke University Medical Center, DUMC Box 3179, Durham, NC 27710. Tel.: 919-681-8422; Fax: 919-668-1599; E-mail: tcreazzo{at}duke.edu.

This report provides a detailed analysis of developmental changes in cytoplasmic free calcium (Ca2+) buffering and excitation-contraction coupling in embryonic chick ventricular myocytes. The peak magnitude of field-stimulated Ca2+ transients declined by 41% between embryonic day (ED) 5 and 15, with most of the decline occurring between ED5 and 11. This was due primarily to a decrease in Ca2+ currents. Sarcoplasmic reticulum (SR) Ca2+ content increased 14-fold from ED5 to 15. Ca2+ transients in voltage-clamped myocytes after blockade of SR function permitted computation of the fast Ca buffer power of the cytosol as expressed as generalized values of Bmax and KD. Bmax rose with development whereas KD did not change significantly. The computed SR Ca2+ contribution to the Ca2+ transient and gain factor for Ca2+-induced Ca2+ release increased markedly between ED5 and 11 and slightly thereafter. These results paralleled the maturation of SR and peripheral couplings reported by others and demonstrated a strong relationship between structure and function in development of excitation-contraction coupling. Modeling of buffer power from estimates of the major cytosolic Ca binding moieties yielded a Bmax and KD in reasonable agreement with experiment. From ED5 to 15, troponin C was the major Ca2+ binding moiety, followed by SR and calmodulin.




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