title: Renal sodium transport in renin-deficient Dahl salt-sensitive rats.
abstract: OBJECTIVE
  The Dahl salt-sensitive rat is a well-established model of salt-sensitive hypertension. The goal of this study was to assess the expression and activity of renal sodium channels and transporters in the renin-deficient salt-sensitive rat.
  
  
  METHODS
  Renin knockout (Ren(-/-)) rats created on the salt-sensitive rat background were used to investigate the role of renin in the regulation of ion transport in salt-sensitive hypertension. Western blotting and patch-clamp analyses were utilized to assess the expression level and activity of Na(+) transporters.
  
  
  RESULTS
  It has been described previously that Ren(-/-) rats exhibit severe kidney underdevelopment, polyuria, and lower body weight and blood pressure compared to their wild-type littermates. Here we found that renin deficiency led to decreased expression of sodium-hydrogen antiporter (NHE3), the Na(+)/H(+) exchanger involved in Na(+) absorption in the proximal tubules, but did not affect the expression of Na-K-Cl cotransporter (NKCC2), the main transporter in the loop of Henle. In the distal nephron, the expression of sodium chloride cotransporter (NCC) was lower in Ren(-/-) rats. Single-channel patch clamp analysis detected decreased ENaC activity in Ren(-/-) rats which was mediated via changes in the channel open probability.
  
  
  CONCLUSIONS
  These data illustrate that renin deficiency leads to significant dysregulation of ion transporters.
authors.affiliation: Department of Physiology, Medical College of Wisconsin, USA.
authors.forename: Tengis S
authors.initials: TS
authors.lastname: Pavlov
authors.affiliation: Department of Physiology, Medical College of Wisconsin, USA.
authors.forename: Vladislav
authors.initials: V
authors.lastname: Levchenko
authors.affiliation: Department of Physiology, Medical College of Wisconsin, USA.
authors.forename: Daria V
authors.initials: DV
authors.lastname: Ilatovskaya
authors.affiliation: Department of Physiology, Medical College of Wisconsin, USA Cardiovascular and Metabolic Diseases, MedImmune, Cambridge, UK.
authors.forename: Carol
authors.initials: C
authors.lastname: Moreno
authors.affiliation: Department of Physiology, Medical College of Wisconsin, USA Cardiovascular Center, Medical College of Wisconsin, USA staruschenko@mcw.edu.
authors.forename: Alexander
authors.initials: A
authors.lastname: Staruschenko
mesh_terms: D000450:Aldosterone / Q000097:blood; D000818:Animals; D001692:Biological Transport; D015153:Blotting, Western; D003345:Corticosterone / Q000097:blood; D004573:Electrolytes / Q000097:blood; D053503:Epithelial Sodium Channels / Q000378:metabolism; D007668:Kidney / Q000378:metabolism* / Q000473:pathology; D026901:Membrane Transport Proteins / Q000378:metabolism; D018408:Patch-Clamp Techniques; D020303:Rats, Inbred Dahl; D012083:Renin / Q000172:deficiency* / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*
chemical_list: D004573:Electrolytes; D053503:Epithelial Sodium Channels; D026901:Membrane Transport Proteins; D000450:Aldosterone; D012964:Sodium; D012083:Renin; D003345:Corticosterone
keywords: Na-K-Cl cotransporter; Renin-angiotensin-aldosterone system; aldosterone-sensitive distal nephron; epithelial sodium channel; sodium chloride cotransporter; sodium-hydrogen antiporter