title: Effect of angiotensin-converting enzyme inhibition on myocardial vascularization in the adolescent and adult spontaneously hypertensive rat.
abstract: OBJECTIVE
  To determine whether angiotensin-converting enzyme (ACE) inhibition treatment enhances myocardial vascularization in adolescent and adult spontaneously hypertensive rats (SHRs).
  
  
  METHODS
  Male SHRs were treated from 7 to 14 or from 16 to 24 weeks of age with the ACE inhibitor, perindopril, in either a low dose (0.1 mg/kg per day) or a high dose (1 mg/kg per day). Some rats were concomitantly treated with a bradykinin antagonist. At termination of treatment, the left ventricular wall was extensively sampled and the surface area density and length density of myocardial blood vessels stereologically determined.
  
  
  RESULTS
  High-dose perindopril treatment prevented the development of hypertension and left ventricular hypertrophy in adolescent SHRs and markedly reduced blood pressure and left ventricular size in adult SHRs. SHRs treated with the low dose of perindopril remained hypertensive, although there were significant reductions in blood pressure and left ventricular growth. High-dose perindopril treatment in adolescent SHRs led to a significant increase in the surface area density of blood vessels in the left ventricle after 4 weeks of treatment and an increase in both the surface area density and length density of blood vessels after 7 weeks of treatment Co-administration with the bradykinin antagonist did not reverse these effects. In contrast, ACE inhibitor treatment had no effect on myocardial vascularization in adult rats with established hypertension.
  
  
  CONCLUSIONS
  ACE inhibitor treatment enhances vascularization in the adolescent heart through reductions in myocardial mass, but not capillary growth. ACE inhibition in the adult heart with established hypertension reduces left ventricular hypertrophy, but does not enhance myocardial capillarization.
authors.affiliation: Department of Anatomy and Cell Biology, Monash University, Victoria, Clayton, Australia. Jane.Black@med.monach.edu.au
authors.forename: M J
authors.initials: MJ
authors.lastname: Black
authors.forename: J F
authors.initials: JF
authors.lastname: Bertram
authors.forename: C I
authors.initials: CI
authors.lastname: Johnston
mesh_terms: D000375:Aging / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002196:Capillaries / Q000187:drug effects / Q000254:growth & development; D003326:Coronary Circulation / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D006321:Heart / Q000254:growth & development; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology* / Q000517:prevention & control; D017379:Hypertrophy, Left Ventricular / Q000517:prevention & control; D020913:Perindopril / Q000494:pharmacology*; D051381:Rats; D011918:Rats, Inbred SHR / Q000033:anatomy & histology / Q000502:physiology*; D011921:Rats, Inbred WKY; D012016:Reference Values; D013599:Systole; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D020913:Perindopril