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10.1681/ASN.2016090935 http://scihub22266oqcxt.onion/10.1681/ASN.2016090935 28052988!5461801!28052988     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2017 ; 28 (6): 1814-1825 Nephropedia Template TP {{tp|p=28052988|t=2017. Potassium Sensing by Renal Distal Tubules Requires Kir4 1 |pdf=|usr=}}{{28052988}} gab.com Text Potassium Sensing by Renal Distal Tubules Requires Kir4 1 JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=28052988 #FOAvip The mammalian distal convoluted tubule (DCT) makes an important contribution to potassium homeostasis by modulating NaCl transport. The thiazide-sensitive Na(+)/Cl(-) cotransporter (NCC) is activated by low potassium intake and by hypokalemia. Coupled with suppression of aldosterone secretion, activation of NCC helps to retain potassium by increasing electroneutral NaCl reabsorption, therefore reducing Na(+)/K(+) exchange. Yet the mechanisms by which DCT cells sense plasma potassium concentration and transmit the information to the apical membrane are not clear. Here, we tested the hypothesis that the potassium channel Kir4.1 is the potassium sensor of DCT cells. We generated mice in which Kir4.1 could be deleted in the kidney after the mice are fully developed. Deletion of Kir4.1 in these mice led to moderate salt wasting, low BP, and profound potassium wasting. Basolateral membranes of DCT cells were depolarized, nearly devoid of conductive potassium transport, and unresponsive to plasma potassium concentration. Although renal WNK4 abundance increased after Kir4.1 deletion, NCC abundance and function decreased, suggesting that membrane depolarization uncouples WNK kinases from NCC. Together, these results indicate that Kir4.1 mediates potassium sensing by DCT cells and couples this signal to apical transport processes. Twit Text FOAVip Potassium Sensing by Renal Distal Tubules Requires Kir4 1 ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=28052988 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28052988 #FOAvip English Wikipedia <ref>{{Cite pmid|28052988}}</ref> Potassium Sensing by Renal Distal Tubules Requires Kir4 1 #MMPMID28052988 Cuevas CA; Su XT; Wang MX; Terker AS; Lin DH; McCormick JA; Yang CL; Ellison DH; Wang WH J Am Soc Nephrol 2017[Jun]; 28 (6): 1814-1825 PMID28052988show ga The mammalian distal convoluted tubule (DCT) makes an important contribution to potassium homeostasis by modulating NaCl transport. The thiazide-sensitive Na(+)/Cl(-) cotransporter (NCC) is activated by low potassium intake and by hypokalemia. Coupled with suppression of aldosterone secretion, activation of NCC helps to retain potassium by increasing electroneutral NaCl reabsorption, therefore reducing Na(+)/K(+) exchange. Yet the mechanisms by which DCT cells sense plasma potassium concentration and transmit the information to the apical membrane are not clear. Here, we tested the hypothesis that the potassium channel Kir4.1 is the potassium sensor of DCT cells. We generated mice in which Kir4.1 could be deleted in the kidney after the mice are fully developed. Deletion of Kir4.1 in these mice led to moderate salt wasting, low BP, and profound potassium wasting. Basolateral membranes of DCT cells were depolarized, nearly devoid of conductive potassium transport, and unresponsive to plasma potassium concentration. Although renal WNK4 abundance increased after Kir4.1 deletion, NCC abundance and function decreased, suggesting that membrane depolarization uncouples WNK kinases from NCC. Together, these results indicate that Kir4.1 mediates potassium sensing by DCT cells and couples this signal to apical transport processes. |*Potassium[MESH] |Animals[MESH] |Kidney Tubules, Distal/cytology/*physiology[MESH] |Mice[MESH]Potassium Sensing by Renal Distal Tubules Requires Kir4 1 (epmc).pdf DeepDyve Pubget Overpricing