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Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation
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| Zeitschriftentitel: | American Journal of Physiology-Renal Physiology |
|---|---|
| Personen und Körperschaften: | , |
| In: | American Journal of Physiology-Renal Physiology, 305, 2013, 4, S. F427-F438 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Wall, Susan M. Weinstein, Alan M. Wall, Susan M. Weinstein, Alan M. |
|---|---|
| author |
Wall, Susan M. Weinstein, Alan M. |
| spellingShingle |
Wall, Susan M. Weinstein, Alan M. American Journal of Physiology-Renal Physiology Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation Physiology |
| author_sort |
wall, susan m. |
| spelling |
Wall, Susan M. Weinstein, Alan M. 1931-857X 1522-1466 American Physiological Society Physiology http://dx.doi.org/10.1152/ajprenal.00022.2013 <jats:p>Renal intercalated cells mediate the secretion or absorption of Cl<jats:sup>−</jats:sup>and OH<jats:sup>−</jats:sup>/H<jats:sup>+</jats:sup>equivalents in the connecting segment (CNT) and cortical collecting duct (CCD). In so doing, they regulate acid-base balance, vascular volume, and blood pressure. Cl<jats:sup>−</jats:sup>absorption is either electrogenic and amiloride-sensitive or electroneutral and thiazide-sensitive. However, which Cl<jats:sup>−</jats:sup>transporter(s) are targeted by these diuretics is debated. While epithelial Na<jats:sup>+</jats:sup>channel (ENaC) does not transport Cl<jats:sup>−</jats:sup>, it modulates Cl<jats:sup>−</jats:sup>transport probably by generating a lumen-negative voltage, which drives Cl<jats:sup>−</jats:sup>flux across tight junctions. In addition, recent evidence indicates that ENaC inhibition increases electrogenic Cl<jats:sup>−</jats:sup>secretion via a type A intercalated cells. During ENaC blockade, Cl<jats:sup>−</jats:sup>is taken up across the basolateral membrane through the Na<jats:sup>+</jats:sup>-K<jats:sup>+</jats:sup>−2Cl<jats:sup>−</jats:sup>cotransporter (NKCC1) and then secreted across the apical membrane through a conductive pathway (a Cl<jats:sup>−</jats:sup>channel or an electrogenic exchanger). The mechanism of this apical Cl<jats:sup>−</jats:sup>secretion is unresolved. In contrast, thiazide diuretics inhibit electroneutral Cl<jats:sup>−</jats:sup>absorption mediated by a Na<jats:sup>+</jats:sup>-dependent Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>exchanger. The relative contribution of the thiazide and the amiloride-sensitive components of Cl<jats:sup>−</jats:sup>absorption varies between studies and probably depends on the treatment model employed. Cl<jats:sup>−</jats:sup>absorption increases markedly with angiotensin and aldosterone administration, largely by upregulating the Na<jats:sup>+</jats:sup>-independent Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>exchanger pendrin. In the absence of pendrin [ Slc26a4<jats:sup>(−/−)</jats:sup>or pendrin null mice], aldosterone-stimulated Cl<jats:sup>−</jats:sup>absorption is significantly reduced, which attenuates the pressor response to this steroid hormone. Pendrin also modulates aldosterone-induced changes in ENaC abundance and function through a kidney-specific mechanism that does not involve changes in the concentration of a circulating hormone. Instead, pendrin changes ENaC abundance and function, at least in part, by altering luminal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>. This review summarizes mechanisms of Cl<jats:sup>−</jats:sup>transport in CNT and CCD and how these transporters contribute to the regulation of extracellular volume and blood pressure.</jats:p> Cortical distal nephron Cl<sup>−</sup>transport in volume homeostasis and blood pressure regulation American Journal of Physiology-Renal Physiology |
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10.1152/ajprenal.00022.2013 |
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Online Free |
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Biologie |
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American Physiological Society, 2013 |
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American Physiological Society, 2013 |
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1522-1466 1931-857X |
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wall2013corticaldistalnephroncltransportinvolumehomeostasisandbloodpressureregulation |
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2013 |
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American Physiological Society |
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ai |
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ai |
| series |
American Journal of Physiology-Renal Physiology |
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49 |
| title |
Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_unstemmed |
Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_full |
Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_fullStr |
Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_full_unstemmed |
Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_short |
Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_sort |
cortical distal nephron cl<sup>−</sup>transport in volume homeostasis and blood pressure regulation |
| topic |
Physiology |
| url |
http://dx.doi.org/10.1152/ajprenal.00022.2013 |
| publishDate |
2013 |
| physical |
F427-F438 |
| description |
<jats:p>Renal intercalated cells mediate the secretion or absorption of Cl<jats:sup>−</jats:sup>and OH<jats:sup>−</jats:sup>/H<jats:sup>+</jats:sup>equivalents in the connecting segment (CNT) and cortical collecting duct (CCD). In so doing, they regulate acid-base balance, vascular volume, and blood pressure. Cl<jats:sup>−</jats:sup>absorption is either electrogenic and amiloride-sensitive or electroneutral and thiazide-sensitive. However, which Cl<jats:sup>−</jats:sup>transporter(s) are targeted by these diuretics is debated. While epithelial Na<jats:sup>+</jats:sup>channel (ENaC) does not transport Cl<jats:sup>−</jats:sup>, it modulates Cl<jats:sup>−</jats:sup>transport probably by generating a lumen-negative voltage, which drives Cl<jats:sup>−</jats:sup>flux across tight junctions. In addition, recent evidence indicates that ENaC inhibition increases electrogenic Cl<jats:sup>−</jats:sup>secretion via a type A intercalated cells. During ENaC blockade, Cl<jats:sup>−</jats:sup>is taken up across the basolateral membrane through the Na<jats:sup>+</jats:sup>-K<jats:sup>+</jats:sup>−2Cl<jats:sup>−</jats:sup>cotransporter (NKCC1) and then secreted across the apical membrane through a conductive pathway (a Cl<jats:sup>−</jats:sup>channel or an electrogenic exchanger). The mechanism of this apical Cl<jats:sup>−</jats:sup>secretion is unresolved. In contrast, thiazide diuretics inhibit electroneutral Cl<jats:sup>−</jats:sup>absorption mediated by a Na<jats:sup>+</jats:sup>-dependent Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>exchanger. The relative contribution of the thiazide and the amiloride-sensitive components of Cl<jats:sup>−</jats:sup>absorption varies between studies and probably depends on the treatment model employed. Cl<jats:sup>−</jats:sup>absorption increases markedly with angiotensin and aldosterone administration, largely by upregulating the Na<jats:sup>+</jats:sup>-independent Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>exchanger pendrin. In the absence of pendrin [ Slc26a4<jats:sup>(−/−)</jats:sup>or pendrin null mice], aldosterone-stimulated Cl<jats:sup>−</jats:sup>absorption is significantly reduced, which attenuates the pressor response to this steroid hormone. Pendrin also modulates aldosterone-induced changes in ENaC abundance and function through a kidney-specific mechanism that does not involve changes in the concentration of a circulating hormone. Instead, pendrin changes ENaC abundance and function, at least in part, by altering luminal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>. This review summarizes mechanisms of Cl<jats:sup>−</jats:sup>transport in CNT and CCD and how these transporters contribute to the regulation of extracellular volume and blood pressure.</jats:p> |
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| description | <jats:p>Renal intercalated cells mediate the secretion or absorption of Cl<jats:sup>−</jats:sup>and OH<jats:sup>−</jats:sup>/H<jats:sup>+</jats:sup>equivalents in the connecting segment (CNT) and cortical collecting duct (CCD). In so doing, they regulate acid-base balance, vascular volume, and blood pressure. Cl<jats:sup>−</jats:sup>absorption is either electrogenic and amiloride-sensitive or electroneutral and thiazide-sensitive. However, which Cl<jats:sup>−</jats:sup>transporter(s) are targeted by these diuretics is debated. While epithelial Na<jats:sup>+</jats:sup>channel (ENaC) does not transport Cl<jats:sup>−</jats:sup>, it modulates Cl<jats:sup>−</jats:sup>transport probably by generating a lumen-negative voltage, which drives Cl<jats:sup>−</jats:sup>flux across tight junctions. In addition, recent evidence indicates that ENaC inhibition increases electrogenic Cl<jats:sup>−</jats:sup>secretion via a type A intercalated cells. During ENaC blockade, Cl<jats:sup>−</jats:sup>is taken up across the basolateral membrane through the Na<jats:sup>+</jats:sup>-K<jats:sup>+</jats:sup>−2Cl<jats:sup>−</jats:sup>cotransporter (NKCC1) and then secreted across the apical membrane through a conductive pathway (a Cl<jats:sup>−</jats:sup>channel or an electrogenic exchanger). The mechanism of this apical Cl<jats:sup>−</jats:sup>secretion is unresolved. In contrast, thiazide diuretics inhibit electroneutral Cl<jats:sup>−</jats:sup>absorption mediated by a Na<jats:sup>+</jats:sup>-dependent Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>exchanger. The relative contribution of the thiazide and the amiloride-sensitive components of Cl<jats:sup>−</jats:sup>absorption varies between studies and probably depends on the treatment model employed. Cl<jats:sup>−</jats:sup>absorption increases markedly with angiotensin and aldosterone administration, largely by upregulating the Na<jats:sup>+</jats:sup>-independent Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>exchanger pendrin. In the absence of pendrin [ Slc26a4<jats:sup>(−/−)</jats:sup>or pendrin null mice], aldosterone-stimulated Cl<jats:sup>−</jats:sup>absorption is significantly reduced, which attenuates the pressor response to this steroid hormone. Pendrin also modulates aldosterone-induced changes in ENaC abundance and function through a kidney-specific mechanism that does not involve changes in the concentration of a circulating hormone. Instead, pendrin changes ENaC abundance and function, at least in part, by altering luminal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>. This review summarizes mechanisms of Cl<jats:sup>−</jats:sup>transport in CNT and CCD and how these transporters contribute to the regulation of extracellular volume and blood pressure.</jats:p> |
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| spelling | Wall, Susan M. Weinstein, Alan M. 1931-857X 1522-1466 American Physiological Society Physiology http://dx.doi.org/10.1152/ajprenal.00022.2013 <jats:p>Renal intercalated cells mediate the secretion or absorption of Cl<jats:sup>−</jats:sup>and OH<jats:sup>−</jats:sup>/H<jats:sup>+</jats:sup>equivalents in the connecting segment (CNT) and cortical collecting duct (CCD). In so doing, they regulate acid-base balance, vascular volume, and blood pressure. Cl<jats:sup>−</jats:sup>absorption is either electrogenic and amiloride-sensitive or electroneutral and thiazide-sensitive. However, which Cl<jats:sup>−</jats:sup>transporter(s) are targeted by these diuretics is debated. While epithelial Na<jats:sup>+</jats:sup>channel (ENaC) does not transport Cl<jats:sup>−</jats:sup>, it modulates Cl<jats:sup>−</jats:sup>transport probably by generating a lumen-negative voltage, which drives Cl<jats:sup>−</jats:sup>flux across tight junctions. In addition, recent evidence indicates that ENaC inhibition increases electrogenic Cl<jats:sup>−</jats:sup>secretion via a type A intercalated cells. During ENaC blockade, Cl<jats:sup>−</jats:sup>is taken up across the basolateral membrane through the Na<jats:sup>+</jats:sup>-K<jats:sup>+</jats:sup>−2Cl<jats:sup>−</jats:sup>cotransporter (NKCC1) and then secreted across the apical membrane through a conductive pathway (a Cl<jats:sup>−</jats:sup>channel or an electrogenic exchanger). The mechanism of this apical Cl<jats:sup>−</jats:sup>secretion is unresolved. In contrast, thiazide diuretics inhibit electroneutral Cl<jats:sup>−</jats:sup>absorption mediated by a Na<jats:sup>+</jats:sup>-dependent Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>exchanger. The relative contribution of the thiazide and the amiloride-sensitive components of Cl<jats:sup>−</jats:sup>absorption varies between studies and probably depends on the treatment model employed. Cl<jats:sup>−</jats:sup>absorption increases markedly with angiotensin and aldosterone administration, largely by upregulating the Na<jats:sup>+</jats:sup>-independent Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>exchanger pendrin. In the absence of pendrin [ Slc26a4<jats:sup>(−/−)</jats:sup>or pendrin null mice], aldosterone-stimulated Cl<jats:sup>−</jats:sup>absorption is significantly reduced, which attenuates the pressor response to this steroid hormone. Pendrin also modulates aldosterone-induced changes in ENaC abundance and function through a kidney-specific mechanism that does not involve changes in the concentration of a circulating hormone. Instead, pendrin changes ENaC abundance and function, at least in part, by altering luminal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>. This review summarizes mechanisms of Cl<jats:sup>−</jats:sup>transport in CNT and CCD and how these transporters contribute to the regulation of extracellular volume and blood pressure.</jats:p> Cortical distal nephron Cl<sup>−</sup>transport in volume homeostasis and blood pressure regulation American Journal of Physiology-Renal Physiology |
| spellingShingle | Wall, Susan M., Weinstein, Alan M., American Journal of Physiology-Renal Physiology, Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation, Physiology |
| title | Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_full | Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_fullStr | Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_full_unstemmed | Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_short | Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| title_sort | cortical distal nephron cl<sup>−</sup>transport in volume homeostasis and blood pressure regulation |
| title_unstemmed | Cortical distal nephron Cl−transport in volume homeostasis and blood pressure regulation |
| topic | Physiology |
| url | http://dx.doi.org/10.1152/ajprenal.00022.2013 |