title: Increased expression of Na,K-ATPase and a selective increase in phosphorylation at Ser-11 in the cortex of the 2-kidney, 1-clip hypertensive rat.
abstract: BACKGROUND
  The mechanism by which blood pressure increases during renovascular hypertension is incompletely understood. We, therefore, tested the hypothesis that in the 2-kidney, 1-clip (2K-1C) rat, in which hypertension develops due to increased angiotensin II (Ang II) levels, there is increased expression and phosphorylation of Na,K-ATPase at Ser-11 and Ser-18 in the kidney cortex. The rationale is Ang II is reported to directly stimulate Na,K-ATPase activity in proximal tubules, which reabsorb 2/3 of filtered sodium, via increased phosphorylation at Ser-11 and Ser-18 and the Na,K-ATPase drives sodium reabsorption.
  
  
  METHODS
  Five-week-old Sprague-Dawley rats underwent unilateral or sham clipping of the right renal artery and placement of telemetry transmitters. Six weeks later blood pressure and plasma Ang II were measured and kidneys harvested. The amount of Na,K-ATPase, phosphorylation at Ser-11 and Ser-18, and the expression of β-actin in each kidney cortex were measured by quantitative immunoblotting.
  
  
  RESULTS
  Clipping significantly increased mean arterial pressure from 110 ± 3 to 148 ± 13 mm Hg, plasma Ang II, cortical Na,K-ATPase in the unclipped kidney of 2K-1C compared to sham-clipped rats, the total cortical Na,K-ATPase in both kidneys compared to sham-clipped rats, and the extent to which the Na,K-ATPase was phosphorylated at Ser-11. Clipping did not significantly change phosphorylation at Ser-18, β-actin, or the total protein in the cortexes of both kidneys.
  
  
  CONCLUSIONS
  Thus, in the kidney cortex of rats with renovascular hypertension there is increased expression of Na,K-ATPase and a selective increase in its phosphorylation at Ser-11 that could increase the capacity to reabsorb sodium and water.
authors.affiliation: Department of Physiology, Wayne State University, School of Medicine, Detroit, Michigan, USA.
authors.forename: Lauren
authors.initials: L
authors.lastname: Kava
authors.forename: Noreen F
authors.initials: NF
authors.lastname: Rossi
authors.forename: Raymond
authors.initials: R
authors.lastname: Mattingly
authors.forename: Douglas R
authors.initials: DR
authors.lastname: Yingst
mesh_terms: D000199:Actins; D000595:Amino Acid Sequence; D000804:Angiotensin II / Q000097:blood* / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003251:Constriction, Pathologic; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D007672:Kidney Cortex / Q000378:metabolism*; D007687:Kidney Tubules, Proximal / Q000378:metabolism; D008297:Male; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012077:Renal Artery / Q000473:pathology; D012694:Serine / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000096:biosynthesis*
chemical_list: D000199:Actins; D000804:Angiotensin II; D012694:Serine; D000254:Sodium-Potassium-Exchanging ATPase