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1)Soleimani M. SLC26 Cl(-)/HCO3(-) exchangers in the kidney: roles in health and disease. Kidney Int. 2013; 84: 657-66
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2)Everett LA, Glaser B, Beck JC, et al. Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS). Nat Genet. 1997; 17 : 411-22
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3)Wall SM, Weinstein AM. Cortical distal nephron Cl- transport in volume homeostasis and blood pressure regulation. Am J Physiol Renal Physiol. 2013; 305: F427-38
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4)Royaux IE, Wall SM, Karniski LP, et al. Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretion. Proc Natl Acad Sci U S A. 2001; 98: 4221-6
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5)Amlal H, Petrovic S, Xu J, et al. Deletion of the anion exchanger Slc26a4 (pendrin) decreases apical Cl(-)/HCO3(-) exchanger activity and impairs bicarbonate secretion in kidney collecting duct. Am J Physiol Cell Physiol. 2010; 299: C33-41
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6)Verlander JW, Hassell KA, Royaux IE, et al. Deoxycorticosterone upregulates PDS (Slc26a4) in mouse kidney: role of pendrin in mineralocorticoid-induced hypertension. Hypertension. 2003; 42: 356-62
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7)Wall SM, Kim YH, Stanley L, et al. NaCl restriction upregulates renal Slc26a4 through subcellular redistribution: role in Cl- conservation. Hypertension. 2004; 44: 982-7
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8)Kandasamy N, Fugazzola L, Evans M, et al. Life-threatening metabolic alkalosis in Pendred syndrome. Eur J Endocrinol. 2011; 165: 167-70
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9)Kim YH, Pech V, Spencer KB, et al. Reduced ENaC protein abundance contributes to the lower blood pressure observed in pendrin-null mice. Am J Physiol Renal Physiol. 2007; 293: F1314-24
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10)Leviel F, Hübner CA, Houillier P, et al. The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. J Clin Invest. 2010; 120: 1627-35
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11)Schultheis PJ, Lorenz JN, Meneton P, et al. Phenotype resembling Gitelman’s syndrome in mice lacking the apical Na+-Cl− cotransporter of the distal convoluted tubule. J Biol Chem. 1998; 273: 29150-5
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12)Soleimani M, Barone S, Xu J, et al. Double knockout of pendrin and Na-Cl cotransporter (NCC) causes severe salt wasting, volume depletion, and renal failure. Proc Natl Acad Sci U S A. 2012; 109: 13368-73
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13)Pela I, Bigozzi M, Bianchi B. Profound hypokalemia and hypochloremic metabolic alkalosis during thiazide therapy in a child with Pendred syndrome. Clin Nephrol. 2008; 69: 450-3
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14)Nomura N, Tajima M, Sugawara N, et al. Generation and analyses of R8L barttin knockin mouse. Am J Physiol Renal Physiol. 2011; 301: F297-307
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15)Quentin F, Chambrey R, Trinh-Trang-Tan MM, et al. The Cl−/HCO3− exchanger pendrin in the rat kidney is regulated in response to chronic alterations in chloride balance. Am J Physiol Renal Physiol. 2004; 287: F1179-88
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16)Wang Z, Wang T, Petrovic S, et al. Renal and intestinal transport defects in Slc26a6-null mice. Am J Physiol Cell Physiol. 2005; 288: C957-65
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17)Singh AK, Amlal H, Haas PJ, et al. Fructose-induced hypertension: essential role of chloride and fructose absorbing transporters PAT1 and Glut5. Kidney Int. 2008; 74: 438-47
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18)Soleimani M. Dietary fructose, salt absorption and hypertension in metabolic syndrome: towards a new paradigm. Acta Physiol (Oxf). 2011; 201: 55-62
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19)Amlal H, Xu J, Barone S, et al. The chloride channel/transporter Slc26a9 regulates the systemic arterial pressure and renal chloride excretion. J Mol Med (Berl). 2013; 91: 561-72
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20)Matsumura Y, Uchida S, Kondo Y, et al. Overt nephrogenic diabetes insipidus in mice lacking the CLC-K1 chloride channel. Nat Genet. 1999; 21: 95-8
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21)Simon D, Bindra R, Mansfield T, et al. Mutations in the chloride channel gene, CLCNKB, cause Bartter’s syndrome type III. Nat Genet. 1997; 17: 171-8
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22)Birkenhäger R, Otto E, Schürmann M, et al. Mutation of BSND causes Bartter syndrome with sensorineural deafness and kidney failure. Nat Genet. 2001; 29: 310-4
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23)Estévez R, Boettger T, Stein V, et al. Barttin is a Cl− channel beta-subunit crucial for renal Cl− reabsorption and inner ear K+ secretion. Nature. 2001; 414: 558-61
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24)Rickheit G, Maier H, Strenzke N, et al. Endocochlear potential depends on Cl− channels: mechanism underlying deafness in Bartter syndrome IV. EMBO J. 2008; 27: 2907-17
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25)Jeck N, Waldegger P, Doroszewicz J, et al. A common sequence variation of the CLCNKB gene strongly activates ClC-Kb chloride channel activity. Kidney Int. 2004; 65: 190-7
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26)Jeck N, Waldegger S, Lampert A, et al. Activating mutation of the renal epithelial chloride channel ClC-Kb predisposing to hypertension. Hypertension. 2004; 43: 1175-81
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27)Sile S, Velez DR, Gillani NB, et al. CLCNKB-T481S and essential hypertension in a Ghanaian population. J Hypertens. 2009; 27: 298-304
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28)Barlassina C, Dal Fiume C, Lanzani C, et al. Common genetic variants and haplotypes in renal CLCNKA gene are associated to salt-sensitive hypertension. Hum Mol Genet. 2007; 16: 1630-8
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29)Fava C, Montagnana M, Almgren P, et al. The functional variant of the CLC-Kb channel T481S is not associated with blood pressure or hypertension in Swedes. J Hypertens. 2007; 25: 111-6
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30)Chang PY, Zhang XG, Su XL. Lack of association of variants of the renal salt reabsorption-related genes SLC12A3 and ClC-Kb and hypertension in Mongolian and Han populations in Inner Mongolia. Genet Mol Res. 2011; 10: 948-54
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31)Liantonio A, Gramegna G, Camerino GM, et al. In-vivo administration of CLC-K kidney chloride channels inhibitors increases water diuresis in rats: a new drug target for hypertension? J Hypertens. 2012; 30: 153-67
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