title: Angiotensin-converting enzyme inhibition reduces lipid deposits in myocardium and improves left ventricular function of obese zucker rats.
abstract: OBJECTIVE
  Alterations in the renin angiotensin system, cardiac lipotoxicity, and left ventricular (LV) dysfunction have been reported in obese rats. The present study examined whether angiotensin-converting enzyme inhibition could ameliorate lipid deposition and ventricular function in the myocardium of obese Zucker rats (OZRs).
  
  
  METHODS
  For 6 months, rats were treated as follows: Group (G) 1, OZR, no treatment; G2, OZR + ramipril (R); G3, OZR + amlodipine (AML); and G4, lean Zucker rats. LV function was assessed by echocardiogram and lipid deposits in cardiomyocytes (LDCM) by light microscopy using Oil red O.
  
  
  RESULTS
  At the end of the experiment, both OZR + R and OZR + AML groups presented similar reduction in blood pressure in comparison with untreated OZR (p < 0.01). OZR with R presented lower insulin-to-glucose ratio and lower serum triglycerides and cholesterol when compared with both untreated OZR and OZR with AML (p < 0.01). Fractional shortening by echocardiogram was as follows: G1, 25.4 +/- 3.8 (vs. G2 and G4, p < 0.05); G2, 37.2 +/- 2.4; G3, 29.3 +/- 4.4 (vs. G2 and G4, p < 0.05); and G4, 40.8 +/- 2.3. Percentage LDCM was as follows: G1, 12.4 +/- 2.7 (vs. G2 and G4, p < 0.05); G2, 0.8 +/- 0.2; G3, 11.1 +/- 2.1 (vs. G2 and G4, p < 0.05); and G4, 0.1 +/- 0.1. There was a negative correlation between fractional shortening and LDCM percentage in OZR (r = -0.93) and in OZR + AML (r = -0.87).
  
  
  CONCLUSIONS
  AML reduced blood pressure significantly; however, it failed to modify both metabolic parameters and LDCM. In contrast, R showed a substantial reduction in LDCM, together with LV function preservation.
authors.affiliation: Laboratory of Experimental Medicine, Hospital Alemán, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina. jtoblli@hospitalaleman.com
authors.forename: Jorge Eduardo
authors.initials: JE
authors.lastname: Toblli
authors.forename: Gabriel
authors.initials: G
authors.lastname: Cao
authors.forename: Carlos
authors.initials: C
authors.lastname: Rivas
authors.forename: Graciela
authors.initials: G
authors.lastname: DeRosa
authors.forename: Patricia
authors.initials: P
authors.lastname: Domecq
mesh_terms: D017311:Amlodipine / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D002784:Cholesterol / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D050356:Lipid Metabolism / Q000187:drug effects*; D008297:Male; D017257:Ramipril / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D011924:Rats, Zucker; D014280:Triglycerides / Q000097:blood; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides; D017311:Amlodipine; D002784:Cholesterol; D017257:Ramipril