title: Effects of Restoration of Blood Flow on the Development of Aortic Atherosclerosis in ApoE-/- Mice With Unilateral Renal Artery Stenosis.
abstract: BACKGROUND
  Chronic unilateral renal artery stenosis (RAS) causes accelerated atherosclerosis in apolipoprotein E-deficient (ApoE(-/-)) mice, but effects of restoration of renal blood flow on aortic atherosclerosis are unknown.
  
  
  RESULTS
  Male ApoE(-/-) mice underwent sham surgery (n=16) or had partial ligation of the right renal artery (n=41) with the ligature being removed 4 days later (D4LR; n=6), 8 days later (D8LR; n=11), or left in place for 90 days (chronic RAS; n=24). Ligature removal at 4 or 8 days resulted in improved renal blood flow, decreased plasma angiotensin II levels, a return of systolic blood pressure to baseline, and increased plasma levels of neutrophil gelatinase associated lipocalin. Chronic RAS resulted in increased lipid staining in the aortic arch (33.2% [24.4, 47.5] vs 11.6% [6.1, 14.2]; P<0.05) and descending thoracic aorta (10.2% [6.4, 25.9] vs 4.9% [2.8, 7.8]; P<0.05), compared to sham surgery. There was an increased amount of aortic arch lipid staining in the D8LR group (22.7% [22.1, 32.7]), compared to sham-surgery, but less than observed with chronic RAS. Lipid staining in the aortic arch was not increased in the D4LR group, and lipid staining in the descending aorta was not increased in either the D8LR or D4LR groups. There was less macrophage expression in infrarenal aortic atheroma in the D4LR and D8LR groups compared to the chronic RAS group.
  
  
  CONCLUSIONS
  Restoration of renal blood flow at either 4 or 8 days after unilateral RAS had a beneficial effect on systolic blood pressure, aortic lipid deposition, and atheroma inflammation.
authors.affiliation: McAllister Heart Institute, University of North Carolina, Chapel Hill, NC.
authors.forename: Alokkumar S
authors.initials: AS
authors.lastname: Pathak
authors.affiliation: McAllister Heart Institute, University of North Carolina, Chapel Hill, NC.
authors.forename: Jianhua
authors.initials: J
authors.lastname: Huang
authors.affiliation: McAllister Heart Institute, University of North Carolina, Chapel Hill, NC.
authors.forename: Mauricio
authors.initials: M
authors.lastname: Rojas
authors.affiliation: Department of Medicine, Duke University, Durham, NC.
authors.forename: Taylor C
authors.initials: TC
authors.lastname: Bazemore
authors.affiliation: McAllister Heart Institute, University of North Carolina, Chapel Hill, NC Division of Cardiology, University of North Carolina, Chapel Hill, NC.
authors.forename: Ruihai
authors.initials: R
authors.lastname: Zhou
authors.affiliation: McAllister Heart Institute, University of North Carolina, Chapel Hill, NC Division of Cardiology, University of North Carolina, Chapel Hill, NC rick_stouffer@med.unc.edu.
authors.forename: George A
authors.initials: GA
authors.lastname: Stouffer
mesh_terms: D000818:Animals; D001018:Aortic Diseases / Q000209:etiology* / Q000503:physiopathology; D001057:Apolipoproteins E / Q000235:genetics / Q000502:physiology*; D050197:Atherosclerosis / Q000209:etiology* / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D058226:Plaque, Atherosclerotic / Q000209:etiology / Q000503:physiopathology; D012078:Renal Artery Obstruction / Q000150:complications* / Q000503:physiopathology
chemical_list: D001057:Apolipoproteins E
keywords: atherosclerosis; hypertension; inflammation; renal; renal artery stenosis