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10.1152/ajprenal.00062.2012 http://scihub22266oqcxt.onion/10.1152/ajprenal.00062.2012 22647633!3423110!22647633     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2012 ; 303 (4): F483-91 Nephropedia Template TP {{tp|p=22647633|t=2012. Differential effects of extracellular ATP on chloride transport in cortical collecting duct cells |pdf=|usr=}}{{22647633}} gab.com Text Differential effects of extracellular ATP on chloride transport in cortical collecting duct cells JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=22647633 #FOAvip Extracellular ATP in the cortical collecting duct can inhibit epithelial sodium channels (ENaC) but also stimulate calcium-activated chloride channels (CACC). The relationship between ATP-mediated regulation of ENaC and CACC activity in cortical collecting duct cells has not been clearly defined. We used the mpkCCD(c14) cortical collecting duct cell line to determine effects of ATP on sodium (Na(+)) and chloride (Cl(-)) transport with an Ussing chamber system. ATP, at a concentration of 10(-6) M or less, did not inhibit ENaC-mediated short-circuit current (I(sc)) but instead stimulated a transient increase in I(sc). The macroscopic current-voltage relationship for ATP-inducible current demonstrated that the direction of this ATP response changes from positive to negative when transepithelial voltage (V(te)) is clamped to less than -10 mV. We hypothesized that this negative V(te) might be found under conditions of aldosterone stimulation. We next stimulated mpkCCD(c14) cells with aldosterone (10(-6) M) and then clamped the V(te) to -50 mV, the V(te) of aldosterone-stimulated cells under open-circuit conditions. ATP (10(-6) M) induced a transient increase in negative clamp current, which could be inhibited by flufenamic acid (CACC inhibitor) and BAPTA-AM (calcium chelator), suggesting that ATP stimulates Cl(-) absorption through CACC. Together, our findings suggest that the status of ENaC activity, by controlling V(te), may dictate the direction of ATP-stimulated Cl(-) transport. This interplay between aldosterone and purinergic signaling pathways may be relevant for regulating NaCl transport in cortical collecting duct cells under different states of extracellular fluid volume. Twit Text FOAVip Differential effects of extracellular ATP on chloride transport in cortical collecting duct cells ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=22647633 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22647633 #FOAvip English Wikipedia <ref>{{Cite pmid|22647633}}</ref> Differential effects of extracellular ATP on chloride transport in cortical collecting duct cells #MMPMID22647633 Rajagopal M; Kathpalia PP; Widdicombe JH; Pao AC Am J Physiol Renal Physiol 2012[Aug]; 303 (4): F483-91 PMID22647633show ga Extracellular ATP in the cortical collecting duct can inhibit epithelial sodium channels (ENaC) but also stimulate calcium-activated chloride channels (CACC). The relationship between ATP-mediated regulation of ENaC and CACC activity in cortical collecting duct cells has not been clearly defined. We used the mpkCCD(c14) cortical collecting duct cell line to determine effects of ATP on sodium (Na(+)) and chloride (Cl(-)) transport with an Ussing chamber system. ATP, at a concentration of 10(-6) M or less, did not inhibit ENaC-mediated short-circuit current (I(sc)) but instead stimulated a transient increase in I(sc). The macroscopic current-voltage relationship for ATP-inducible current demonstrated that the direction of this ATP response changes from positive to negative when transepithelial voltage (V(te)) is clamped to less than -10 mV. We hypothesized that this negative V(te) might be found under conditions of aldosterone stimulation. We next stimulated mpkCCD(c14) cells with aldosterone (10(-6) M) and then clamped the V(te) to -50 mV, the V(te) of aldosterone-stimulated cells under open-circuit conditions. ATP (10(-6) M) induced a transient increase in negative clamp current, which could be inhibited by flufenamic acid (CACC inhibitor) and BAPTA-AM (calcium chelator), suggesting that ATP stimulates Cl(-) absorption through CACC. Together, our findings suggest that the status of ENaC activity, by controlling V(te), may dictate the direction of ATP-stimulated Cl(-) transport. This interplay between aldosterone and purinergic signaling pathways may be relevant for regulating NaCl transport in cortical collecting duct cells under different states of extracellular fluid volume. |Absorptiometry, Photon[MESH] |Adenosine Triphosphate/genetics/*metabolism[MESH] |Animals[MESH] |Anoctamin-1[MESH] |Bestrophins[MESH] |Biological Transport/physiology[MESH] |Cell Line[MESH] |Chloride Channels/genetics/metabolism[MESH] |Chlorides/*metabolism[MESH] |Epithelial Sodium Channels/genetics/metabolism[MESH] |Eye Proteins/genetics/metabolism[MESH] |Gene Expression Regulation[MESH] |Kidney Cortex/*cytology[MESH] |Kidney Tubules, Collecting/*cytology[MESH] |Mice[MESH] |Neoplasm Proteins/genetics/metabolism[MESH]Differential effects of extracellular ATP on chloride transport in cor(epmc).pdf DeepDyve Pubget Overpricing