title: Involvement of vascular angiotensin II-forming enzymes in the progression of aortic abdominal aneurysms in angiotensin II- infused ApoE-deficient mice.
abstract: OBJECTIVE
  Angiotensin (Ang) II-induced abdominal aortic aneurysm (AAA) in apoE-deficient mice has been used as a model of human AAA, but it has been unclear why the progression of AAA continues after stopping the Ang II infusion. The involvement of vascular Ang II-forming enzymes in the progression of AAA was studied.
  
  
  METHODS
  ApoE-deficient mice were infused with Ang II (1,000 ng/kg/min) for 4 weeks and evaluated until 20 weeks after the Ang II infusion. Just after and 20 weeks after stopping the Ang II infusion, the degree of AAA, as well as the ACE and chymase activities, was evaluated. An Ang II receptor blocker (candesartan, 30 mg/kg/day) and an angiotensin-converting enzyme (ACE) inhibitor (lisinopril, 60 mg/kg/day) were given for 20 weeks after stopping the Ang II infusion.
  
  
  RESULTS
  The aortic diameter expanded just after stopping the Ang II infusion and progressed for a further 20 weeks after the infusion was stopped. Just after stopping the infusion, aortic ACE and chymase activities were significantly increased, but only the increase in chymase activity continued until 20 weeks after the infusion was stopped. Candesartan and lisinopril significantly attenuated aortic diameter expansion.
  
  
  CONCLUSIONS
  The increases in vascular Ang II-forming activities were involved in the progression of AAA after stopping the Ang II infusion.
authors: Department of Pharmacology, Osaka Medical College, Osaka 569-8686, Japan.
authors: Nao
authors: N
authors: Inoue
authors: Michiko
authors: M
authors: Muramatsu
authors: Denan
authors: D
authors: Jin
authors: Shinji
authors: S
authors: Takai
authors: Tetsuya
authors: T
authors: Hayashi
authors: Hiroshi
authors: H
authors: Katayama
authors: Yasushi
authors: Y
authors: Kitaura
authors: Hiroshi
authors: H
authors: Tamai
authors: Mizuo
authors: M
authors: Miyazaki
mesh_terms: D000804:Angiotensin II / Q000633:toxicity*; D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D001011:Aorta / Q000201:enzymology; D017544:Aortic Aneurysm, Abdominal / Q000139:chemically induced / Q000473:pathology*; D001057:Apolipoproteins E / Q000172:deficiency; D001562:Benzimidazoles / Q000494:pharmacology; D001713:Biphenyl Compounds; D053818:Chymases / Q000502:physiology*; D018450:Disease Progression; D017706:Lisinopril / Q000494:pharmacology; D051379:Mice; D018345:Mice, Knockout; D007703:Peptidyl-Dipeptidase A / Q000502:physiology*; D013777:Tetrazoles / Q000494:pharmacology
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D001057:Apolipoproteins E; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D013777:Tetrazoles; D000804:Angiotensin II; D017706:Lisinopril; D007703:Peptidyl-Dipeptidase A; D053818:Chymases; C081643:candesartan