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The renal Na + ‐driven Cl ‐ HCO 3 ‐ exchanger SLC4A8 is important for maintaining sodium balance (892.36)
Author(s) -
Jayat Maximilien,
Sinning Anne,
Gerth Melanie,
Calderon Carolina,
Cornière Nicolas,
Baron Stéphanie,
Hadchouel Juliette,
Eladari Dominique,
Hubner Christian,
Chambrey Régine
Publication year - 2014
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.28.1_supplement.892.36
Subject(s) - pendrin , chemistry , endocrinology , medicine , sodium , renin–angiotensin system , blood pressure , kidney , biochemistry , transporter , biology , organic chemistry , gene
We recently described a novel renal NaCl transport system expressed in intercalated cells of the cortical collecting duct (CCD) that results from the parallel action of the Cl‐/HCO3‐ exchanger pendrin and the Na+‐driven Cl‐/HCO3‐ exchanger (NDCBE/ Slc4a8). Even though a role for pendrin in maintaining Na+ balance, normal vascular volume and blood pressure is well documented, there is no direct evidence for such a role for NDCBE yet. We first demonstrated that NDCBE protein was upregulated by primary or secondary hyperaldosteronism, two situations known to increase renal NaCl absorption. Ndcbe deficient mice exhibited hallmarks of vascular dehydration as evident from increased renin mRNA expression and plasma renin activity and developed marked secondary hyperaldosteronism when subjected to NaCl restriction. Systolic blood pressure was lower in Ndcbe deficient mice fed either a normal or NaCl‐free diet and was normalized with a high salt diet, indicating that the lower blood pressure in Ndcbe deficient mice is the consequence of a decreased vascular volume. Since Ndcbe disruption was compensated by an increase in NCC expression and activity, we generated double Ncc/Ndcbe knock‐out mice. Volume depletion in these mice was more pronounced although expression of other major renal Na+ transporters was markedly increased. Taken together, these results demonstrate that NDCBE is critical in maintaining sodium balance, normal vascular volume and blood pressure.