Sodium potassium adenosine triphosphatase activity in preterm and term infants and its possible role in sodium homeostasis during maturation

Citation
T. Bistritzer et al., Sodium potassium adenosine triphosphatase activity in preterm and term infants and its possible role in sodium homeostasis during maturation, ARCH DIS CH, 81(3), 1999, pp. F184-F187
Citations number
38
Categorie Soggetti
Pediatrics,"Medical Research General Topics
Journal title
ARCHIVES OF DISEASE IN CHILDHOOD
ISSN journal
00039888 → ACNP
Volume
81
Issue
3
Year of publication
1999
Pages
F184 - F187
Database
ISI
SICI code
0003-9888(199911)81:3<F184:SPATAI>2.0.ZU;2-T
Abstract
Aim-To investigate sodium (NA(+)) potassium (K+) adenosine triphosphatase ( ATPase) activity in newborn infants at different gestational ages, to eluci date the mechanism underlying poor renal sodium conservation in preterm inf ants. Methods-Fifty three healthy newborn infants, gestational age 30-42 weeks, w ere studied. Umbilical cord red blood cell Na+ K(+)ATPase activity, plasma renin activity, and plasma aldosterone activities were measured in all of t hem. Red blood cell Na(+)K(+)ATPase activity was reexamined in eight preter m infants, one and two weeks after birth. Total and ouabain sensitive ATPas e activity was measured spectrophotometrically using a method that couples ATP hydrolysis with NADH oxidation. Results-Red blood cell Na(+)K(+)ATPase activity was significantly lower (p< 0.01) in preterm babies with a gestational age below 35 weeks, compared wit h those with aged 35 weeks and above: 2.3 (0.8) and 6.7 (1.3) nmol NADH/min ute/mg protein, respectively. There was no correlation between gestational age, Na(+)K(+)ATPase, plasma renin activity and aldosterone values either i n the preterm or term babies. Two weeks after birth, irrespective of gestat ional age, the enzyme activity of the preterm babies increased to values si milar to those observed in the term neonates at birth. Conclusion-The differences in sodium homeostasis between term and preterm b abies are modulated via changes in Na(+)K(+)ATPase activity.