title: Placental oxidative stress in malnourished rats and changes in kidney proximal tubule sodium ATPases in offspring.
abstract: 1. Intrauterine malnutrition has been linked to the development of adult cardiovascular and renal diseases, which are related to altered Na(+) balance. Here we investigated whether maternal malnutrition increases placental oxidative stress with subsequent impact on renal ATP-dependent Na(+) transporters in the offspring. 2. Maternal malnutrition was induced in rats during pregnancy by using a basic regional diet available in north-eastern Brazil. Placental oxidative stress was evaluated by measuring thiobarbituric acid-reactive substances, which were 35-40% higher in malnourished dams (MalN). Na(+) pumps were evaluated in control and prenatally malnourished rats (at 25 and 90 days of age). 3. Identical Na(+)/K(+)-ATPase activity was found in both groups at 25 days (approximately 150 nmol P(i)/mg per min). However, although Na(+)/K(+)-ATPase increased by 40% with growth in control rats, it remained constant in pups from MalN. 4. In juvenile rats, the activity of the ouabain-insensitive Na(+)-ATPase was higher in MalN than in controls (70 vs 25 nmol P(i)/mg per min). Nevertheless, activity did not increase with kidney and body growth: at 90 days, it was 50% lower in MalN than in controls. The maximal stimulation of the Na(+)-ATPase by angiotensin (Ang) II was 35% lower in MalN than in control rats and was attained only with a much higher concentration of the peptide (10(-10) mol/L) than in controls (10(-14) mol/L). 5. Protein kinase C activity, which mediates the effects of AngII on Na(+)-ATPase was only one-third of normal values in the MalN group. 6. These results indicate that placental oxidative stress may contribute to fetal undernutrition, which leads to later disturbances in Na(+) pumps from proximal tubule cells.
authors.affiliation: Department of Physiology and Pharmacology, Federal University of Pernambuco, Recife, Brazil.
authors.forename: Leucio D
authors.initials: LD
authors.lastname: Vieira-Filho
authors.forename: Lucienne S
authors.initials: LS
authors.lastname: Lara
authors.forename: Paulo A
authors.initials: PA
authors.lastname: Silva
authors.forename: Ricardo
authors.initials: R
authors.lastname: Luzardo
authors.forename: Marcelo
authors.initials: M
authors.lastname: Einicker-Lamas
authors.forename: Henriqueta D
authors.initials: HD
authors.lastname: Cardoso
authors.forename: Ana D O
authors.initials: AD
authors.lastname: Paixão
authors.forename: Adalberto
authors.initials: A
authors.lastname: Vieyra
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D027682:Cation Transport Proteins / Q000378:metabolism*; D005260:Female; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D008297:Male; D044342:Malnutrition / Q000378:metabolism*; D008431:Maternal-Fetal Exchange; D018384:Oxidative Stress; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D027682:Cation Transport Proteins; D017392:Thiobarbituric Acid Reactive Substances; D000804:Angiotensin II; D011493:Protein Kinase C; D000251:Adenosine Triphosphatases; C021838:sodium-translocating ATPase; D000254:Sodium-Potassium-Exchanging ATPase