Document Detail


The chloride channel/transporter Slc26a9 regulates the systemic arterial pressure and renal chloride excretion.
MedLine Citation:
PMID:  23149824     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Apical chloride secretory pathways in the kidney medullary collecting duct are thought to play an important role in the modulation of final urine composition and regulation of systemic vascular volume and/or blood pressure. However, the molecular identity of these molecules has largely remained unknown. Here, we demonstrate that Slc26a9, an electrogenic chloride channel/transporter, is localized on the apical membrane of principal cells in the kidney medullary collecting duct and mediates chloride secretion. Mice with the genetic deletion of Slc26a9 show significant reduction in renal chloride excretion when fed a diet high in salt or subjected to water deprivation. Arterial pressure measurements indicated that Slc26a9 knockout (Slc26a9(-/-)) mice are hypertensive under baseline conditions and increase their blood pressure further within 48 h of switching to a high-salt diet. These results suggest that Slc26a9 plays an important role in renal chloride/fluid excretion and arterial pressure regulation. We propose that impaired SLC26A9 activity in humans may interfere with the excretion of excess salt and result in hypertension.
Authors:
Hassane Amlal; Jie Xu; Sharon Barone; Kamyar Zahedi; Manoocher Soleimani
Related Documents :
11116054 - Hypercholesterolemia superimposed by experimental hypertension induces differential dis...
25072354 - Hypotensive and antihypertensive potential of 4-[(1-phenyl-1h-pyrazol-4-yl) methyl]1-pi...
19107804 - Thermomechanical properties, collapse pressure, and expansion of shape memory polymer n...
23600794 - Reactive oxygen species, vascular noxs and hypertension: focus on translational and cli...
2518654 - Treatment of hypertension based on both systolic and diastolic pressure could influence...
7921524 - Evaluation of fentanyl and sufentanil on the diameter of the common bile duct by ultras...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-11-13
Journal Detail:
Title:  Journal of molecular medicine (Berlin, Germany)     Volume:  -     ISSN:  1432-1440     ISO Abbreviation:  J. Mol. Med.     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-11-14     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9504370     Medline TA:  J Mol Med (Berl)     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Research Services, Veterans Affairs Medical Center, Cincinnati, OH, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Negative regulatory responses to metabolically triggered inflammation impair renal epithelial immuni...
Next Document:  Direct rAAV SOX9 administration for durable articular cartilage repair with delayed terminal differe...