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AJP - Heart and Circulatory Physiology, Vol 273, Issue 2 837-H846, Copyright © 1997 by American Physiological Society
ARTICLES |
P. S. Haddock, W. A. Coetzee and M. Artman
Department of Pediatrics, New York University Medical Center, New York 10016, USA.
Previous studies suggesting a greater functional role of cardiac Na+/Ca2+ exchange at birth were performed using tightly buffered free cytosolic Ca2+ concentration ([Ca2+]i). Because Na+/Ca2+ exchange current (INaCa) is influenced by physiological fluctuations in [Ca2+]i, we used conditions of minimally buffered [Ca2+]i to simultaneously record INaCa and cell contractions in single ventricular myocytes isolated from 1 to 27-day-old and adult rabbits. With conventional Cl(-)-containing solutions. Ni(2+)-sensitive outward and inward charge movements were unbalanced, suggesting the presence of a contaminating current (presumably the Ca(2+)-activated Cl- current). Removing Cl- abolished this discrepancy in all age groups and allowed for the accurate quantitation of INaCa. Under Cl(-)-free conditions, outward and inward charge movements were high at birth (4 days: 0.42 +/- 0.03 and -0.38 +/- 0.04 pC/pF, respectively) and decreased postnatally (adult: 0.08 +/- 0.01 and -0.07 +/- 0.01 pC/pF, respectively). Newborn but not adult myocytes contracted during depolarizations in the presence of nifedipine, ryanodine, and thapsigargin. The magnitudes of outward charge movement (Ca2+ influx) and cell shortening exhibited similar voltage dependence, consistent with INaCa-mediated contractions. These results indicate that INaCa can directly support contraction in newborn rabbit ventricular myocytes.
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