title: Effects of enalapril and hydralazine treatment and withdrawal upon cardiovascular hypertrophy in stroke-prone spontaneously hypertensive rats.
abstract: OBJECTIVE
  To test the hypothesis that effects of angiotensin converting enzyme (ACE) inhibitors upon resistance vessel structure are responsible for their ability to cause long-term reduction in blood pressure.
  
  
  METHODS
  Stroke-prone spontaneously hypertensive (SHRSP) and Wistar-Kyoto (WKY) rats were treated with enalapril or hydralazine from 4 to 15 weeks of age. Effects upon tail-cuff blood pressure, left ventricular hypertrophy and structural indices of the superior mesenteric artery (SMA) and its resistance vessels were assessed at 11 weeks of treatment and up to 11 weeks post-treatment.
  
  
  METHODS
  Left ventricular hypertrophy was assessed by left ventricular weight:body weight ratios. Evidence of vascular structural change was obtained from tissue weight:body weight ratios, levels of RNA, DNA and expression of alpha-actin and elastin messenger (m)RNA.
  
  
  RESULTS
  The effects of enalapril and hydralazine upon left ventricular hypertrophy in SHRSP were consistent with their respective effects upon blood pressure. Both drugs prevented the development of medial hypertrophy in SMA and resistance vessels. This was accompanied by substantial reductions in RNA:DNA ratios. Alpha-actin mRNA levels were not affected by either drug but elastin mRNA levels were reduced by both drugs. During the first 12 days post-treatment there was evidence of structural change in SMA accompanying the increases in blood pressure but importantly not in the resistance vessels.
  
  
  CONCLUSIONS
  The effects of enalapril upon left ventricular hypertrophy and mesenteric arterial hypertrophy are totally consistent with responses to blood pressure and the persistence of structural changes post-treatment does not underlie the ability of the ACE inhibitors to persistently suppress hypertension.
authors.affiliation: Commonwealth Scientific and Industrial Research Organization (CSIRO) Division of Human Nutrition, Adelaide, Australia.
authors.forename: R A
authors.initials: RA
authors.lastname: King
authors.forename: R M
authors.initials: RM
authors.lastname: Smith
authors.forename: R
authors.initials: R
authors.lastname: Krishnan
authors.forename: E G
authors.initials: EG
authors.lastname: Cleary
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D004247:DNA / Q000032:analysis; D004549:Elastin / Q000737:chemistry; D004656:Enalapril / Q000494:pharmacology*; D006352:Heart Ventricles / Q000473:pathology; D006830:Hydralazine / Q000494:pharmacology*; D006973:Hypertension / Q000150:complications*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D017538:Mesenteric Artery, Superior / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D009929:Organ Size / Q000187:drug effects; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D012333:RNA, Messenger; D006830:Hydralazine; D004656:Enalapril; D004247:DNA; D004549:Elastin