Contribution of the Na+-K+-2Cl−cotransporter NKCC1 to Cl−secretion in rat OMCD

Wall, Susan M.; Fischer, Michael P.; Mehta, Pramod S.; Hassell, Kathryn A.; Park, Stanley J.

doi:10.1152/ajprenal.2001.280.5.f913

Cited by 46 publications

(46 citation statements)

References 44 publications

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“…5 Tubules were perfused in vitro using the solution above. 5 Cl Ϫ concentration was measured fluorimetrically 13 in collected perfusate samples. Cl Ϫ flux, J Cl , was calculated as described previously.…”

Section: Morphometric Analysismentioning

confidence: 99%

“…Cl Ϫ flux, J Cl , was calculated as described previously. 13 Net fluid transport was taken to be zero. 5 …”

Section: Morphometric Analysismentioning

confidence: 99%

“…[12][13][14] Across intercalated cells, aldosterone stimulates Cl Ϫ absorption through apical Cl Ϫ /HCO 3 Ϫ exchange in series with a basolateral Cl Ϫ conductance. 14 Thus, it is likely that aldosterone analogues activate Slc26a4-mediated apical Cl Ϫ uptake in type B and in non-A, non-B intercalated cells.…”

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confidence: 99%

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NaCl Restriction Upregulates Renal Slc26a4 Through Subcellular Redistribution

et al. 2004

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Abstract-Slc26a4 (Pds, pendrin) is an anion transporter expressed in the apical region of type B and non-A, non-B intercalated cells of the distal nephron. It is upregulated by aldosterone analogues and is critical in the development of mineralocorticoid-induced hypertension. Thus, Slc26a4 expression and its role in blood pressure and fluid and electrolyte homeostasis was explored during NaCl restriction, a treatment model in which aldosterone is appropriately increased. Ultrastructural immunolocalization, balance studies, and cortical collecting ducts (CCDs) perfused in vitro were used. With moderate physiological NaCl restriction, Slc26a4 expression in the apical plasma membrane increased 2-to 3-fold in type B intercalated cells. Because Slc26a4 transports Cl Ϫ , we tested whether NaCl balance differs in Slc26a4 (ϩ/ϩ) (Ϫ/Ϫ) mice had evidence of relative vascular volume depletion because they had a higher arterial pH, hematocrit, and blood urea nitrogen than wild-type mice. With moderate NaCl restriction, blood pressure was similar in Slc26a4 (ϩ/ϩ) and Slc26a4 (Ϫ/Ϫ) mice. However, on a severely restricted intake of NaCl, Slc26a4 (Ϫ/Ϫ) mice were hypotensive relative to wild-type mice. We conclude that Slc26a4 is upregulated with NaCl restriction and is critical in the maintenance of acid-base balance and in the renal conservation of Cl Ϫ and water during NaCl restriction.

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Section: Morphometric Analysismentioning

confidence: 99%

“…Cl Ϫ flux, J Cl , was calculated as described previously. 13 Net fluid transport was taken to be zero. 5 …”

Section: Morphometric Analysismentioning

confidence: 99%

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NaCl Restriction Upregulates Renal Slc26a4 Through Subcellular Redistribution

et al. 2004

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“…These mechanisms may be functionally and molecularly distinct. Detailed studies by Susan Wall and colleagues demonstrated several uptake mechanisms for ammonium on the basolateral side, namely Na + /K + /2Cl --cotransport, possibly NKKC1, and Na + /K + -ATPase (204,206). In both cases NH 4 + can be transported instead of potassium.…”

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Regulated acid–base transport in the collecting duct

Wagner

Devuyst

Bourgeois

et al. 2009

Pflugers Arch - Eur J Physiol

161

142

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The renal collecting system serves the fine-tuning of renal acid-base secretion. Acid-secretory type-A intercalated cells secrete protons via a luminally expressed V-type H(+)-ATPase and generate new bicarbonate released by basolateral chloride/bicarbonate exchangers including the AE1 anion exchanger. Efficient proton secretion depends both on the presence of titratable acids (mainly phosphate) and the concomitant secretion of ammonia being titrated to ammonium. Collecting duct ammonium excretion requires the Rhesus protein RhCG as indicated by recent KO studies. Urinary acid secretion by type-A intercalated cells is strongly regulated by various factors among them acid-base status, angiotensin II and aldosterone, and the Calcium-sensing receptor. Moreover, urinary acidification by H(+)-ATPases is modulated indirectly by the activity of the epithelial sodium channel ENaC. Bicarbonate secretion is achieved by non-type-A intercalated cells characterized by the luminal expression of the chloride/bicarbonate exchanger pendrin. Pendrin activity is driven by H(+)-ATPases and may serve both bicarbonate excretion and chloride reabsorption. The activity and expression of pendrin is regulated by different factors including acid-base status, chloride delivery, and angiotensin II and may play a role in NaCl retention and blood pressure regulation. Finally, the relative abundance of type-A and non-type-A intercalated cells may be tightly regulated. Dysregulation of intercalated cell function or abundance causes various syndromes of distal renal tubular acidosis underlining the importance of these processes for acid-base homeostasis.

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“…Ϫ cotransporter 1 (NKCC1) (23), an electroneutral exchanger that localizes to the basolateral membrane of type A intercalated cells in mouse CCDs and outer medullary collecting ducts (8,23,32). When NKCC1 is inhibited, the benzamil-sensitive component of Cl Ϫ absorption falls, although total and benzamil-sensitive V T are unchanged.…”

Section: Channel (Enac) Reduces CLmentioning

confidence: 99%

ENaC inhibition stimulates HCl secretion in the mouse cortical collecting duct. I. Stilbene-sensitive Cl⁻secretion

Nanami

Lazo‐Fernandez

Pech

et al. 2015

American Journal of Physiology-Renal Physiology

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Inhibition of the epithelial Na+ channel (ENaC) reduces Cl− absorption in cortical collecting ducts (CCDs) from aldosterone-treated rats and mice. Since ENaC does not transport Cl−, the purpose of the present study was to explore how ENaC modulates Cl− absorption in mouse CCDs perfused in vitro. Therefore, we measured transepithelial Cl− flux and transepithelial voltage in CCDs perfused in vitro taken from mice that consumed a NaCl-replete diet alone or the diet with aldosterone administered by minipump. We observed that application of an ENaC inhibitor [benzamil (3 μM)] to the luminal fluid unmasks conductive Cl− secretion. During ENaC blockade, this Cl− secretion fell with the application of a nonselective Cl− channel blocker [DIDS (100 μM)] to the perfusate. While single channel recordings of intercalated cell apical membranes in split-open CCDs demonstrated a Cl− channel with properties that resemble the ClC family of Cl− channels, ClC-5 is not the primary pathway for benzamil-sensitive Cl− flux. In conclusion, first, in CCDs from aldosterone-treated mice, most Cl− absorption is benzamil sensitive, and, second, benzamil application stimulates stilbene-sensitive conductive Cl− secretion, which occurs through a ClC-5-independent pathway.

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Contribution of the Na⁺-K⁺-2Cl⁻cotransporter NKCC1 to Cl⁻secretion in rat OMCD

Cited by 46 publications

References 44 publications

NaCl Restriction Upregulates Renal Slc26a4 Through Subcellular Redistribution

NaCl Restriction Upregulates Renal Slc26a4 Through Subcellular Redistribution

Regulated acid–base transport in the collecting duct

ENaC inhibition stimulates HCl secretion in the mouse cortical collecting duct. I. Stilbene-sensitive Cl⁻secretion

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Contribution of the Na+-K+-2Cl−cotransporter NKCC1 to Cl−secretion in rat OMCD

Cited by 46 publications

References 44 publications

NaCl Restriction Upregulates Renal Slc26a4 Through Subcellular Redistribution

NaCl Restriction Upregulates Renal Slc26a4 Through Subcellular Redistribution

Regulated acid–base transport in the collecting duct

ENaC inhibition stimulates HCl secretion in the mouse cortical collecting duct. I. Stilbene-sensitive Cl−secretion

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Contribution of the Na⁺-K⁺-2Cl⁻cotransporter NKCC1 to Cl⁻secretion in rat OMCD

ENaC inhibition stimulates HCl secretion in the mouse cortical collecting duct. I. Stilbene-sensitive Cl⁻secretion