title: An angiotensin-converting enzyme inhibitor, not an angiotensin II type-1 receptor blocker, prevents beta-aminopropionitrile monofumarate-induced aortic dissection in rats.
abstract: OBJECTIVE
  Cystic medial degeneration (CMD) is a histologic abnormality that is common in aortic diseases such as aortic dilation, aneurysm, or dissection. Although little is known about the mechanism underlying CMD, we have previously demonstrated that angiotensin II signaling via angiotensin II type 2 receptor (AT2R) plays a central role in apoptosis of vascular smooth muscle cells (VSMCs) occurring in CMD associated with Marfan syndrome. The aim of this study is to elucidate the role of angiotensin II signaling in THE pathogenesis of aortic diseases associated with CMD.
  
  
  METHODS
  We investigated the effects of angiotensin-converting enzyme inhibitor (ACEI), temocapril (n = 15), angiotensin II receptor type-1 (AT1R) blocker, CS-866 (n = 15), and vehicle control (n = 17) on 0.25% beta-aminopropionitrile monofumarate (BAPN)-induced aortic dissection and histopathologic findings in a rat model.
  
  
  RESULTS
  Temocapril significantly prevented aortic dissection (P <.05), CMD (P <.01), and VSMC apoptosis (P <.01) compared with vehicle control in BAPN-fed rats. However, CS-866 did not show any preventive effect. Reversed transcriptase-polymerase chain reaction demonstrated that expression of both AT1R and AT2R was detected in control rat aortas, and that AT2R expression was significantly upregulated in the aortas of BAPN-fed rats (P <.01). Blood pressure was significantly and equally lowered in both temocapril and CS-866 groups compared with control.
  
  
  CONCLUSIONS
  Differential expression of angiotensin II receptors and AT2R signaling are involved in the pathogenesis of CMD and aortic dissection in BAPN-fed rats. ACEIs might be of clinical value for the prevention and treatment of aortic diseases related to CMD.
mesh_terms: D000629:Aminopropionitrile / Q000009:adverse effects* / Q000031:analogs & derivatives*; D000784:Aortic Dissection / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D001014:Aortic Aneurysm / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D007093:Imidazoles / Q000627:therapeutic use*; D000068557:Olmesartan Medoxomil; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000627:therapeutic use*; D013777:Tetrazoles / Q000627:therapeutic use*; D013841:Thiazepines / Q000627:therapeutic use*
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D007093:Imidazoles; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D013777:Tetrazoles; D013841:Thiazepines; C027243:beta-aminopropionitrile fumarate; D000629:Aminopropionitrile; D000068557:Olmesartan Medoxomil; C055603:temocapril hydrochloride