Renal and cardiac Na+-K +-ATPase and aconitase in a rat model of fetal programming.
Fetal programming of adult disease is an area of research that has gained considerable attention. Epidemiological studies suggest that adverse intrauterine environment in fetal life is associated with a higher incidence of hypertension and coronary disease. Several mechanisms could contribute to these diseases and be regulated in a tissue-specific manner. The Na(+)-K(+)-ATPase, a membrane-bound enzyme, maintains the Na(+) and K(+) gradients across the plasma membrane of animal cells and therefore provides a mechanism for cell function regulation. Furthermore, in an in vitro model of cardiac hypertrophy, a decrease in the activity of the tricarboxylic acid (TCA) cycle enzyme, aconitase, was observed. We have shown that in our model of fetal programming, these two enzymes were regulated differently in heart and kidney of adult females.
Gaudet
Rébecca
R
CHU Sainte-Justine, Mother and Child University Hospital Center, University of Montreal, Montréal, Québec, Canada.
Brochu
Michèle
M
D000154:Aconitate Hydratase / Q000378:metabolism*; D000818:Animals; D015153:Blotting, Western; D002687:Chitin Synthase / Q000378:metabolism; D004591:Electrophoresis, Polyacrylamide Gel; D047109:Fetal Development; D005317:Fetal Growth Retardation; D007668:Kidney / Q000201:enzymology*; D023421:Models, Animal; D009206:Myocardium / Q000201:enzymology*; D051381:Rats; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D002687:Chitin Synthase; D000154:Aconitate Hydratase; D000254:Sodium-Potassium-Exchanging ATPase