Endogenous vasopressin regulates Na-K-ATPase and Na(+)-K(+)-Cl(-) cotransporter rbsc-1 in rat outer medulla.
Previous reports have shown a stimulatory effect of vasopressin (VP) on Na-K-ATPase and rBSC-1 expression and activity. Whether these VP-dependent mechanisms are operating in vivo in physiological conditions as well as in chronic renal failure (CRF) has been less well studied. We measured ATPase expression and activity and rBSC-1 expression in the outer medulla of controls and moderate CRF rats both before and under in vivo inhibition of VP by OPC-31260, a selective V(2)-receptor antagonist. OPC-31260 decreased Na-K-ATPase activity from 11.2 +/- 1.5 to 3.7 +/- 0.8 in controls (P < 0.05) and from 19.0 +/- 0.8 to 2.9 +/- 0.5 micromol P(i). mg protein(-1) x h(-1) in moderate CRF rats (P < 0.05). CRF was associated with a significant increase in Na-K-ATPase activity (P < 0.05). Similarly, CRF was also associated with a significant increase in Na-K-ATPase expression to 164.4 +/- 21.5% compared with controls (P < 0.05), and OPC-31260 decreased Na-K-ATPase expression in both controls and CRF rats to 57.6 +/- 9.5 and 105.3 +/- 10.9%, respectively (P < 0.05). On the other hand, OPC-31260 decreased rBSC-I expression in both controls and CRF rats to 60.8 +/- 6.5 and 30.0 +/- 6.9%, respectively (P < 0.05), and was not influenced by CRF (95.7 +/- 5.2%). We conclude that 1) endogenous VP modulated Na-K-ATPase and rBSC-1 in both controls and CRF; and 2) CRF was associated with increased activity and expression of the Na-K-ATPase in the outer medulla, in contrast to the unaltered expression of the rBSC-1. The data suggest that endogenous VP could participate in the regulation of electrolyte transport at the level of the outer medulla.
Bertuccio
Claudia A
CA
Instituto de Investigaciones Médicas Alfredo Lanari, University of Buenos Aires, 1427 Buenos Aires, Argentina.
Ibarra
Fernando R
FR
Toledo
Jorge E
JE
Arrizurieta
Elvira E
EE
Martin
Rodolfo S
RS
D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001552:Benzazepines / Q000494:pharmacology; D004195:Disease Models, Animal; D007676:Kidney Failure, Chronic / Q000378:metabolism; D007679:Kidney Medulla / Q000737:chemistry / Q000201:enzymology*; D008297:Male; D009088:Mucoproteins / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D017483:Receptors, Vasopressin / Q000378:metabolism; D028021:Sodium-Potassium-Chloride Symporters / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D064466:Solute Carrier Family 12, Member 1; D058949:Uromodulin; D014667:Vasopressins / Q000378:metabolism*; D014882:Water-Electrolyte Balance / Q000502:physiology
D065092:Antidiuretic Hormone Receptor Antagonists; D001552:Benzazepines; D009088:Mucoproteins; D017483:Receptors, Vasopressin; C578716:Slc12a1 protein, rat; D028021:Sodium-Potassium-Chloride Symporters; D064466:Solute Carrier Family 12, Member 1; C548614:Umod protein, rat; D058949:Uromodulin; D014667:Vasopressins; C076251:mozavaptan; D000254:Sodium-Potassium-Exchanging ATPase