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H,K‐ATPase type 2 is required for renal adaptation to pregnancy
Author(s) -
Crambert Gilles,
Doucet Alain,
Salhi Amel
Publication year - 2012
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.26.1_supplement.1103.2
Subject(s) - endocrinology , medicine , gestation , stimulation , reabsorption , kidney , pregnancy , biology , fetus , renal function , excretion , atpase , chemistry , enzyme , biochemistry , genetics
Renal reabsorption of K+ during dietary K+ restriction requires the stimulation of H,K‐ATPase type 2 by adrenal progesterone (Elabida et al. 2011, Kidney Int. 80, 256–262). Since renal K+ retention has been observed during pregnancy we investigated whether this pathway could be functional in this physiological state. During the late part of gestation in mice, the decrease in renal K+ excretion is accompanied by stimulation of HKA2 mRNA and activity. In this condition, kidney function is disconnected from the dietary conditions since gravid mice increase their food consumption (and their K+ intake) by 15%. HKA2‐null mice are unable to efficiently retain K+ during gestation compared to wild‐type littermate (WT) but maintain normal plasma K+ values (around 3.9 mM). This occurs in parallel with a decrease of the fertility rate (86% vs. 25% of successful gestation in WT and HKA2‐null mice, respectively) and a higher mortality rate during gestation in HKA2‐null mice compared to WT. Both phenotypes are reversed when gravid HKA2‐null are given a K+ supplementation in their drinking water. All together, our results provide evidence that pregnancy is a physiological state where kidney is switched from a K+ secretive to a K+ reabsorptive state because of stimulation of H,K‐ATPase type 2. Moreover, inability to do so, have an impact on the development of the gestation.