Altered renal expression of Na(+) transporters and ROMK in protein-deprived rats.
Potassium depletion has been associated with altered sodium reabsorption in tubule segments. We studied if the altered abundance of Na(+) transporters and ROMK are associated with distal potassium secretion that contributes to the development of hypokalemia in protein-deprived rats. After weaning, Wistar rats were fed with a low-protein diet (8%, LP) for 14 days and then recovered with a normal-protein (NP) diet (24%, RP). An age-matched control group was fed with an NP diet (24%, NP). We showed hypokalemia, lower glomerular filtration rate and higher FEK(+) in the LP group. Immunoblotting revealed that the type 3 Na(+)/H(+) exchanger in the cortex was decreased in the LP group. However, the type 2 Na(+)-K(+)-2Cl(-) cotransporter was increased in the outer stripe of the outer medulla in the LP group. The abundance of the aldosterone-regulated Na(+)-Cl(-) cotransporter (NCC) and epithelial Na(+) channel (ENaC) was higher in the LP group and was associated with higher plasma aldosterone level. ROMK protein levels were increased. Na(+)/K(+)-ATPase protein levels were the same in both groups. After the recovery period, the expression of Na(+) transporters and ROMK returned to control values. We conclude that increased expression of NCC, ENaC subunits, and ROMK contributed to distal potassium secretion leading to enhanced potassium excretion, which may explain the hypokalemia resulting from LP feeding. A role of aldosterone may be suggested.
Ruete
María Celeste
MC
IMBECU-CONICET (Consejo Nacional de Investigaciones Científicas y Tecnológicas), Mendoza, Argentina.
Carrizo
Liliana C
LC
Bocanegra
María Victoria
MV
Vallés
Patricia G
PG
D000818:Animals; D018753:Diet, Protein-Restricted / Q000009:adverse effects*; D053503:Epithelial Sodium Channels / Q000378:metabolism; D005260:Female; D007008:Hypokalemia / Q000209:etiology / Q000378:metabolism*; D007668:Kidney / Q000201:enzymology / Q000378:metabolism*; D026901:Membrane Transport Proteins / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D011955:Receptors, Drug / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*; D000074083:Sodium-Hydrogen Exchanger 3; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism; D028021:Sodium-Potassium-Chloride Symporters / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D064466:Solute Carrier Family 12, Member 1; D064486:Solute Carrier Family 12, Member 3; D027981:Symporters / Q000378:metabolism; D015854:Up-Regulation
D053503:Epithelial Sodium Channels; C510692:Kcnj1 protein, rat; D026901:Membrane Transport Proteins; D024661:Potassium Channels, Inwardly Rectifying; D011955:Receptors, Drug; C440894:Scnn1a protein, rat; C507050:Scnn1b protein, rat; C507054:Scnn1g protein, rat; C578716:Slc12a1 protein, rat; C578876:Slc12a3 protein, rat; D000074083:Sodium-Hydrogen Exchanger 3; D017923:Sodium-Hydrogen Exchangers; D028021:Sodium-Potassium-Chloride Symporters; D064466:Solute Carrier Family 12, Member 1; D064486:Solute Carrier Family 12, Member 3; D027981:Symporters; D012964:Sodium; C499075:Atp1a1 protein, rat; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium