Premium
Hyperglycemia, low salt diet, and metabolic acidosis increase the expression of KCl cotransporters in the kidney
Author(s) -
Melo Zesergio,
Bautista Rocio,
CruzRangel Silvia,
Bobadilla Norma,
Gamba Gerardo,
Mercado Adriana
Publication year - 2013
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.27.1_supplement.1210.9
Subject(s) - endocrinology , medicine , cotransporter , sodium , metabolic acidosis , kidney , chemistry , nephron , renal cortex , symporter , acidosis , loop of henle , epithelial polarity , transporter , biology , membrane , biochemistry , gene , organic chemistry
The KCl cotransporter isoforms KCC3 and KCC4 are expressed in several regions of the nephron, but their roles are largely unknown. To begin to understand the renal physiological aspects of KCCs, we evaluated the KCC3 and KCC4 mRNA and protein expression levels (real time RT‐PCR and Western blot, respectively), as well as their intrarenal distribution (confocal microscopy). The studied models in male wistar rats were hyperglycemia, 30 days after a single dose of streptozotocin (60 mg/kg), metabolic acidosis (NH4Cl 150 mM in drinking water during seven days), and low sodium diet (0.1% NaCl diet for seven days). KCC3 expression was significantly increased during hyperglycemia in renal cortex, at the basolateral membrane of proximal tubular cells. In contrast, KCC4 expression was not affected by hyperglycemia, but was significantly increased by low sodium diet, at the basolateral membrane of the thick ascending limb, and by metabolic acidosis in renal medulla, specifically at the basolateral membrane of alfa intercalated cells. These observations support a role for KCC3 in the response of proximal tubules to an increase in glucose concentration in the ultrafiltrate and points out to KCC4 as an exit pathway for potassium and chloride in the thick ascending limb of Henle during low sodium diet and as an important transporter in the response to metabolic acidosis by collecting duct cells.