
| 10.1152/ajprenal.00245.2010
http://scihub22266oqcxt.onion/10.1152/ajprenal.00245.2010
 21123494!3044001!21123494
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Am+J+Physiol+Renal+Physiol 2011 ; 300 (2): F412-24 Nephropedia Template TP
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Oxygen regulation of the epithelial Na channel in the collecting duct #MMPMID21123494Husted RF; Lu H; Sigmund RD; Stokes JBAm J Physiol Renal Physiol 2011[Feb]; 300 (2): F412-24 PMID21123494show ga
The PO(2) within the kidney changes dramatically from cortex to medulla. The present experiments examined the effect of changing PO(2) on epithelial Na channel (ENaC)-mediated Na transport in the collecting duct using the mpkCCD-c14 cell line. Decreasing ambient O(2) concentration from 20 to 8% decreased ENaC activity by 40%; increasing O(2) content to 40% increased ENaC activity by 50%. The O(2) effect required several hours to develop and was not mimicked by the acid pH that developed in monolayers incubated in low-O(2) medium. Corticosteroids increased ENaC activity at each O(2) concentration; there was no interaction. The pathways for O(2) and steroid regulation of ENaC are different since O(2) did not substantially affect Sgk1, alpha-ENaC, Gilz, or Usp2-45 mRNA levels, genes involved in steroid-mediated ENaC regulation. The regulation of ENaC activity by these levels of O(2) appears not to be mediated by changes in hypoxia-inducible factor-1alpha or -2alpha activity or a change in AMP kinase activity. Changes in O(2) concentration had minimal effect on alpha- or gamma-ENaC mRNA and protein levels; there were moderate effects on beta-ENaC levels. However, 40% O(2) induced substantially greater total beta- and gamma-ENaC on the apical surface compared with 8% O(2); both subunits demonstrated a greater increase in the mature forms. The alpha-ENaC subunit was difficult to detect on the apical surface, perhaps because our antibodies do not recognize the major mature form. These results identify a mechanism of ENaC regulation that may be important in different regions of the kidney and in responses to changes in dietary NaCl.|Adenylate Kinase/metabolism[MESH]|Adrenal Cortex Hormones/pharmacology[MESH]|Animals[MESH]|Basic Helix-Loop-Helix Transcription Factors/metabolism[MESH]|Cell Line[MESH]|Epithelial Sodium Channels/drug effects/*metabolism[MESH]|Humans[MESH]|Hydrogen-Ion Concentration[MESH]|Hypoxia-Inducible Factor 1/metabolism[MESH]|Kidney Tubules, Collecting/drug effects/*metabolism[MESH]|Mice[MESH]
  
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