title: Long-term inhibition of the renin-angiotensin system in genetic hypertension: analysis of the impact on blood pressure and cardiovascular structural changes.
abstract: OBJECTIVE
  To compare, using data from published studies, the efficacy of chronic inhibition of the renin-angiotensin system in inducing persistent downregulation of hemodynamic and cardiovascular structural changes in an adult rat with established genetic hypertension with the widely accepted known downregulation in young genetically hypertensive rats.
  
  
  METHODS
  We report on 36 studies that satisfied our inclusion criteria (angiotensin converting enzyme inhibitor or angiotensin II receptor antagonist treatment that lowered arterial pressure levels for at least 3 weeks). Of the 24 studies concerning developing hypertensive rats, a significant number (n = 17) also examined the persistence of any hemodynamic or cardiovascular effects after withdrawal of treatment. Conversely, of 15 studies using adult rats only seven and three reported on post-treatment hemodynamic and cardiovascular structural indices respectively.
  
  
  RESULTS
  During treatment the hemodynamic and cardiovascular structural changes produced were qualitatively and quantitatively similar in the young and adult treated rats. Critical assessment of the persistence of these effects after withdrawal of treatment again found qualitatively similar responses. However, the strength of this finding is limited by the paucity of studies concerning adult rats in which equivalent treatment durations and equipressor doses of treatments were compared between these two age groups.
  
  
  CONCLUSIONS
  Blockade of the renin-angiotensin system appears to have an efficacy in reversing established hypertension and hypertrophy similar to that with which it prevents the development of hypertension and hypertrophy. This partial 'cure' of hypertension after withdrawal of treatment is clearly evident when treatment is initiated during the development of hypertension and appears to be similar even when treatment is initiated in established hypertension.
authors.affiliation: Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada.
authors.forename: M J
authors.initials: MJ
authors.lastname: Lundie
authors.forename: P
authors.initials: P
authors.lastname: Friberg
authors.forename: R L
authors.initials: RL
authors.lastname: Kline
authors.forename: M A
authors.initials: MA
authors.lastname: Adams
mesh_terms: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001808:Blood Vessels / Q000187:drug effects* / Q000473:pathology; D006332:Cardiomegaly / Q000188:drug therapy*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D006984:Hypertrophy; D051381:Rats
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors