title: Induction of apoptosis during development of hypertensive nephrosclerosis.
abstract: BACKGROUND
  As the biology of programmed cell death, or apoptosis, is clarified, a role for this process in the pathophysiology of organ dysfunction and fibrosis has been hypothesized. Hypertensive nephrosclerosis represents an important cause of end-stage renal disease. One model of the progressive, noninflammatory, sclerotic renal lesion of hypertension is the Dahl/Rapp salt-sensitive rat, which was examined in this study.
  
  
  METHODS
  Male, Dahl/Rapp salt-sensitive (SS) and Sprague-Dawley rats were placed on either 0.3 or 8.0% NaCl diets for three weeks. Blood pressure was determined, and the kidneys were harvested for histochemical analysis and to obtain total RNA for RNase protection assays and total protein for Western blotting.
  
  
  RESULTS
  An increase in apoptosis in the glomerular and tubular compartments was observed only in kidneys of SS rats on the high-salt diet. These findings occurred at a time when renal function was markedly impaired and irreversible changes in renal morphology developed. Temporally associated with this increase in apoptosis was augmented expression of pro-apoptotic molecules that included Fas, Bax, and Bcl-XS.
  
  
  CONCLUSIONS
  The inappropriate shift in expression of proteins that facilitate apoptosis in the nephron, along with ongoing cell death that manifested at a time when renal function was deteriorating, supported an important role for this process in development of hypertensive nephrosclerosis.
authors.affiliation: Nephrology Research and Training Center, University of Alabama at Birmingham, 35294-0007, USA.
authors.forename: W Z
authors.initials: WZ
authors.lastname: Ying
authors.forename: P X
authors.initials: PX
authors.lastname: Wang
authors.forename: P W
authors.initials: PW
authors.lastname: Sanders
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D004039:Diet, Sodium-Restricted; D006973:Hypertension / Q000150:complications*; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000503:physiopathology; D007684:Kidney Tubules / Q000503:physiopathology; D008297:Male; D009400:Nephrosclerosis / Q000209:etiology* / Q000503:physiopathology*; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D020303:Rats, Inbred Dahl; D017207:Rats, Sprague-Dawley; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; D019014:fas Receptor / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; C494813:Bcl2l1 protein, rat; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; D019014:fas Receptor