NA-K-ATPase ACTIVITY AND MITOCHONDRIAL FUNCTION IN THE NEWBORN† 1292

Oxygen consumption (QO₂) and ATP synthesis by isolated mitochondria(MITO) increase at birth in liver and kidney (Ped. Res. 37,214) and these changes are prevented by newborn hypoxia. To determine whether increased QO₂ is initiated by increased Na-K-ATPase activity and associated ATP demand pre-term rabbit pups (30-31 days gestation, term=32 days) delivered by C-section were either sacrificed at birth (time zero, TZ) or maintained for 4 hr at 35° C with humidified room air. Kidney (K), heart (H) and cerebral cortex (CC) were harvested from TZ and 4 hr pups to determine MITO QO₂ and Na-K-ATPase activity. Compared to TZ, ADP stimulated QO₂ was higher after birth in K (4.3 ± 1.0 vs 7.5 ± 1.2, nmol O₂/ min/ mg Prot., p < 0.05, n=6) but was unchanged in H (12.7 ± 1.1 vs 12.1± 1.1, n=7) or CC (9.6 ± 1.5 vs 10.2 ± 2.1, n=5). In contrast, Na-K-ATPase activity was lower 4 hr after birth in K (1.2 ± 0.2 vs 0.65 ± 0.27 umol PO₄/ 30 min/ mg prot., p < 0.05, n=6) and H (0.45 ± 0.08 vs 0.13 ± 0.01, p < 0.05, n=3) but not CC(0.63 ± 0.14 vs 0.66 ± 0.09, n=8). Western blot analysis of K homogenates suggest that reduced ATPase activity is not due to lower pump number. When pups were maintained under hypoxic conditions (10% O₂) from birth, K MITO QO₂ and Na-K-ATPase were not different from TZ(n=5). These data demonstrate that changes in Na-K-ATPase activity are not associated with the rapid adaptive change in MITO QO₂ at birth. However, coordinate regulation of QO2 and ATPase activity by O₂ availability was evident in K.