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Alterations in renal sodium and acid‐base transport in H,K‐ATPase null mice
Author(s) -
Greenlee Megan,
Lynch Jeanette,
Rudin Alicia,
Wingo Charles
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1012.4
Subject(s) - chemistry , sodium , acid–base homeostasis , endocrinology , kidney , medicine , gene isoform , atpase , urinary system , excretion , titratable acid , potassium , biochemistry , enzyme , biology , organic chemistry , gene
The kidney expresses two H,K‐ATPase isoforms in the collecting duct, HKα 1 or HKα 2 , that function to transport potassium (K) in exchange for protons, particularly in states of K depletion. However, loss of either HKα 1 or HKα 2 H,K‐ATPase isoforms did not significantly effect either urinary K excretion or systemic acid‐base balance in mice (Spicer et al. J Biol Chem . 2000 275(28); Meneton et al. J Clin Invest . 1998 101(3)). Because another isoform is present in these single knockout animals, we hypothesized that the H,K‐ATPases compensated for each other. To test this hypothesis, the effect of dietary K depletion on renal electrolyte and acid‐base handling was evaluated in double‐knockout mice lacking both HKα 1 or HKα 2 (HKα 1,2 −/‐) . Surprisingly, HKα 1,2 −/− mice efficiently conserved urinary K. However, the HKα 1,2 −/− mice excreted significantly more urinary titratable acid and ammonium, sodium (Na) and chloride (Cl) with no apparent change in blood Na, Cl, pH, or HCO 3 . With K depletion, HKα 1,2 −/− mice retained more urinary Na than wild type mice. The evidence suggests that renal H,K‐ATPases may not play an essential role in net renal K conservation. Instead, the pumps may participate directly or indirectly in both Na and acid‐base transport by the kidney. These studies were supported by an NIH grant (RO1‐DK‐049750).