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J Am Soc Nephrol
2010 Nov 01;2111:1928-41. doi: 10.1681/ASN.2009121257.
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Pendrin modulates ENaC function by changing luminal HCO3-.
Pech V
,
Pham TD
,
Hong S
,
Weinstein AM
,
Spencer KB
,
Duke BJ
,
Walp E
,
Kim YH
,
Sutliff RL
,
Bao HF
,
Eaton DC
,
Wall SM
.
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The epithelial Na(+) channel, ENaC, and the Cl(-)/HCO(3)(-) exchanger, pendrin, mediate NaCl absorption within the cortical collecting duct and the connecting tubule. Although pendrin and ENaC localize to different cell types, ENaC subunit abundance and activity are lower in aldosterone-treated pendrin-null mice relative to wild-type mice. Because pendrin mediates HCO(3)(-) secretion, we asked if increasing distal delivery of HCO(3)(-) through a pendrin-independent mechanism "rescues" ENaC function in pendrin-null mice. We gave aldosterone and NaHCO(3) to increase pendrin-dependent HCO(3)(-) secretion within the connecting tubule and cortical collecting duct, or gave aldosterone and NaHCO(3) plus acetazolamide to increase luminal HCO(3)(-) concentration, [HCO(3)(-)], independent of pendrin. Following treatment with aldosterone and NaHCO(3), pendrin-null mice had lower urinary pH and [HCO(3)(-)] as well as lower renal ENaC abundance and function than wild-type mice. With the addition of acetazolamide, however, acid-base balance as well as ENaC subunit abundance and function was similar in pendrin-null and wild-type mice. We explored whether [HCO(3)(-)] directly alters ENaC abundance and function in cultured mouse principal cells (mpkCCD). Amiloride-sensitive current and ENaC abundance rose with increased [HCO(3)(-)] on the apical or the basolateral side, independent of the substituting anion. However, ENaC was more sensitive to changes in [HCO(3)(-)] on the basolateral side of the monolayer. Moreover, increasing [HCO(3)(-)] on the apical and basolateral side of Xenopus kidney cells increased both ENaC channel density and channel activity. We conclude that pendrin modulates ENaC abundance and function, at least in part by increasing luminal [HCO(3)(-)] and/or pH.
Bailey,
NHE2-mediated bicarbonate reabsorption in the distal tubule of NHE3 null mice.
2004, Pubmed
Bailey,
NHE2-mediated bicarbonate reabsorption in the distal tubule of NHE3 null mice.
2004,
Pubmed
Bens,
Corticosteroid-dependent sodium transport in a novel immortalized mouse collecting duct principal cell line.
1999,
Pubmed
Boudry,
Effect of acid lumen pH on potassium transport in renal cortical collecting tubules.
1976,
Pubmed
Brooks,
Targeted proteomic profiling of renal Na(+) transporter and channel abundances in angiotensin II type 1a receptor knockout mice.
2002,
Pubmed
Buerkert,
Segmental analysis of the renal tubule in buffer production and net acid formation.
1983,
Pubmed
Catalán,
Cftr and ENaC ion channels mediate NaCl absorption in the mouse submandibular gland.
2010,
Pubmed
Chang,
Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1.
1996,
Pubmed
Collier,
Extracellular chloride regulates the epithelial sodium channel.
2009,
Pubmed
,
Xenbase
DuBose,
Effect of carbonic anhydrase inhibition on superficial and deep nephron bicarbonate reabsorption in the rat.
1983,
Pubmed
Everett,
Targeted disruption of mouse Pds provides insight about the inner-ear defects encountered in Pendred syndrome.
2001,
Pubmed
Faroqui,
Metabolic acidosis has dual effects on sodium handling by rat kidney.
2006,
Pubmed
Frische,
Regulated expression of pendrin in rat kidney in response to chronic NH4Cl or NaHCO3 loading.
2003,
Pubmed
Hallows,
Regulation of epithelial Na+ transport by soluble adenylyl cyclase in kidney collecting duct cells.
2009,
Pubmed
,
Xenbase
Hanley,
Study of chloride transport across the rabbit cortical collecting tubule.
1978,
Pubmed
Kemendy,
Aldosterone alters the open probability of amiloride-blockable sodium channels in A6 epithelia.
1992,
Pubmed
Kim,
Long-term regulation of renal Na-dependent cotransporters and ENaC: response to altered acid-base intake.
2000,
Pubmed
Kim,
Immunocytochemical localization of pendrin in intercalated cell subtypes in rat and mouse kidney.
2002,
Pubmed
Kim,
Intercalated cell H+/OH- transporter expression is reduced in Slc26a4 null mice.
2005,
Pubmed
Kim,
Reduced ENaC protein abundance contributes to the lower blood pressure observed in pendrin-null mice.
2007,
Pubmed
Knepper,
Organization of nephron function.
1983,
Pubmed
Marunaka,
Effects of vasopressin and cAMP on single amiloride-blockable Na channels.
1991,
Pubmed
Masilamani,
Aldosterone-mediated regulation of ENaC alpha, beta, and gamma subunit proteins in rat kidney.
1999,
Pubmed
Milton,
Regulation of B-type intercalated cell apical anion exchange activity by CO2/HCO3-.
1998,
Pubmed
Palmer,
Effects of cell Ca and pH on Na channels from rat cortical collecting tubule.
1987,
Pubmed
Pech,
Angiotensin II increases chloride absorption in the cortical collecting duct in mice through a pendrin-dependent mechanism.
2007,
Pubmed
Richardson,
Bicarbonate reabsorption in the papillary collecting duct: effect of acetazolamide.
1982,
Pubmed
Royaux,
Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretion.
2001,
Pubmed
Schuster,
Cyclic adenosine monophosphate-stimulated anion transport in rabbit cortical collecting duct. Kinetics, stoichiometry, and conductive pathways.
1986,
Pubmed
Shimkets,
Liddle's syndrome: heritable human hypertension caused by mutations in the beta subunit of the epithelial sodium channel.
1994,
Pubmed
Shipway,
Biochemical characterization of prostasin, a channel activating protease.
2004,
Pubmed
Snyder,
Minireview: regulation of epithelial Na+ channel trafficking.
2005,
Pubmed
Stanton,
Effects of pH on potassium transport by renal distal tubule.
1982,
Pubmed
Sun,
Decreased expression of Slc26a4 (Pendrin) and Slc26a7 in the kidneys of carbonic anhydrase II-deficient mice.
2008,
Pubmed
Terris,
Long-term regulation of four renal aquaporins in rats.
1996,
Pubmed
Verlander,
Dietary Cl(-) restriction upregulates pendrin expression within the apical plasma membrane of type B intercalated cells.
2006,
Pubmed
Verlander,
Deoxycorticosterone upregulates PDS (Slc26a4) in mouse kidney: role of pendrin in mineralocorticoid-induced hypertension.
2003,
Pubmed
Wall,
Localization of pendrin in mouse kidney.
2003,
Pubmed
Wall,
Hypotension in NKCC1 null mice: role of the kidneys.
2006,
Pubmed
Wall,
NaCl restriction upregulates renal Slc26a4 through subcellular redistribution: role in Cl- conservation.
2004,
Pubmed
Wall,
NH+4 augments net acid secretion by a ouabain-sensitive mechanism in isolated perfused inner medullary collecting ducts.
1996,
Pubmed
Weinstein,
A mathematical model of distal nephron acidification: diuretic effects.
2008,
Pubmed
Yao,
Mice lacking protein kinase C beta present modest increases in systolic blood pressure and NH4Cl-induced metabolic acidosis.
2006,
Pubmed
