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Am J Physiol Cell Physiol 284: C1123-C1132, 2003. First published January 8, 2003; doi:10.1152/ajpcell.00148.2002
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Vol. 284, Issue 5, C1123-C1132, May 2003

Age-related differences in Na+-dependent Ca2+ accumulation in rabbit hearts exposed to hypoxia and acidification

S. E. Anderson, H. Liu, H. S. Ho, E. J. Lewis, and P. M. Cala

Department of Human Physiology, University of California, Davis, California 95616-8644

In this study, we test the hypothesis that in newborn hearts (as in adults) hypoxia and acidification stimulate increased Na+ uptake, in part via pH-regulatory Na+/H+ exchange. Resulting increases in intracellular Na+ (Nai) alter the force driving the Na+/Ca2+ exchanger and lead to increased intracellular Ca2+. NMR spectroscopy measured Nai and cytosolic Ca2+ concentration ([Ca2+]i) and pH (pHi) in isolated, Langendorff-perfused 4- to 7-day-old rabbit hearts. After Na+/K+ ATPase inhibition, hypoxic hearts gained Na+, whereas normoxic controls did not [19 ± 3.4 to 139 ± 14.6 vs. 22 ± 1.9 to 22 ± 2.5 (SE) meq/kg dry wt, respectively]. In normoxic hearts acidified using the NH4Cl prepulse, pHi fell rapidly and recovered, whereas Nai rose from 31 ± 18.2 to 117.7 ± 20.5 meq/kg dry wt. Both protocols caused increases in [Ca]i; however, [Ca]i increased less in newborn hearts than in adults (P < 0.05). Increases in Nai and [Ca]i were inhibited by the Na+/H+ exchange inhibitor methylisobutylamiloride (MIA, 40 µM; P < 0.05), as well as by increasing perfusate osmolarity (+30 mosM) immediately before and during hypoxia (P < 0.05). The data support the hypothesis that in newborn hearts, like adults, increases in Nai and [Ca]i during hypoxia and after normoxic acidification are in large part the result of increased uptake via Na+/H+ and Na+/Ca2+ exchange, respectively. However, for similar hypoxia and acidification protocols, this increase in [Ca]i is less in newborn than adult hearts.

newborn heart; intracellular Na+, Ca2+, and pH


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