title: Role of angiotensin II in early cardiovascular growth and vascular amplifier development in spontaneously hypertensive rats.
abstract: OBJECTIVE
  To examine the role played by angiotensin II (AII) in the development of prehypertensive vascular hypertrophy in the spontaneously hypertensive rat (SHR) and to determine whether normalization of prehypertensive vascular hypertrophy attenuates the development of hypertension.
  
  
  METHODS
  Male SHR and Wistar-Kyoto (WKY) rats were treated from age 10 days until age 6 weeks with perindopril, an angiotensin converting enzyme (ACE) inhibitor, or with losartan, a type 1 AII receptor antagonist.
  
  
  METHODS
  At termination of treatment, or 8 weeks after cessation of treatment, vascular growth was assessed by measurement of hindquarter resistance properties and of the medial cross-sectional area of first-order mesenteric arteries. The growth of the heart was assessed by measurement of the left ventricle:body weight ratio.
  
  
  RESULTS
  Perindopril and losartan treatment of SHR and WKY rats led to a heterogeneous response in the vasculature, resulting in a reduction in perfusion pressures at maximum dilatation and constriction in the hindquarter vasculature but no significant change in medial cross-sectional area of small mesenteric arteries. Neither perindopril nor losartan treatment affected the growth of the left ventricle in the SHR. After the cessation of treatment the development of hypertension in the losartan- and perindopril-treated SHR did not differ from that in controls.
  
  
  CONCLUSIONS
  These results suggest that AII, acting via angiotensin type 1 receptors, plays an important role in determining the early post-natal reactivity of the hindquarter vasculature but not the medial cross-sectional area of the mesenteric vasculature, which implies that different growth regulatory mechanisms are operating in the two vascular beds. The lack of effect in some vascular beds, together with the lack of effect on the heart, may account for the absence of a persistent effect on the blood pressure.
authors.affiliation: Baker Medical Research Institute, Victoria, Australia.
authors.forename: M J
authors.initials: MJ
authors.lastname: Black
authors.forename: P
authors.initials: P
authors.lastname: Kanellakis
authors.forename: A
authors.initials: A
authors.lastname: Bobik
mesh_terms: D000804:Angiotensin II / Q000037:antagonists & inhibitors / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D000831:Animals, Newborn; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D001835:Body Weight / Q000187:drug effects; D006332:Cardiomegaly / Q000517:prevention & control; D002319:Cardiovascular System / Q000187:drug effects / Q000473:pathology*; D006973:Hypertension / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control; D006984:Hypertrophy / Q000517:prevention & control*; D007211:Indoles / Q000494:pharmacology / Q000627:therapeutic use; D007668:Kidney / Q000473:pathology; D019808:Losartan / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D008638:Mesenteric Arteries / Q000033:anatomy & histology / Q000187:drug effects; D009929:Organ Size / Q000187:drug effects; D010208:Papaverine / Q000494:pharmacology; D020913:Perindopril; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D007211:Indoles; D000804:Angiotensin II; D010208:Papaverine; D019808:Losartan; D020913:Perindopril