[Cellular and molecular mechanisms of sodium pump activation in experimental models of nephrotic syndrome].
Edema represent an abnormal expansion of the intersTitial compartment which belong to the extracellular volume. This interstitial expansion is linked to the accumulation of sodium in the extracellular volume due to an imbalance between sodium intake and urinary sodium output. The stimulation of tubular sodium reabsorption is located in the collecting duct where a stimulation of sodium pump hydrolytic activity has been evidenced. The excess of sodium pump hydrolytic activity is associated with an overexpression of the alpha subunit of the sodium pump at the cell surface and a transcriptional induction of alpha and beta sub-units mRNAs. This overexpression is synchronized with the decrease of the final urinary sodium excretion, the positivation of sodium balance and the period of ascites formation.
Deschênes
G
G
Service de néphrologie pédiatrique, Hôpital Armand-Trousseau, Paris.
Feraille
E
E
Doucet
A
A
D000818:Animals; D003404:Creatinine / Q000652:urine; D016623:Ion Pumps / Q000378:metabolism*; D007684:Kidney Tubules / Q000187:drug effects / Q000378:metabolism*; D016014:Linear Models; D009404:Nephrotic Syndrome / Q000139:chemically induced / Q000378:metabolism*; D011692:Puromycin Aminonucleoside / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000378:metabolism* / Q000652:urine
D016623:Ion Pumps; D011692:Puromycin Aminonucleoside; D012964:Sodium; D003404:Creatinine