title: Impaired collateral artery development in spontaneously hypertensive rats.
abstract: OBJECTIVE
  To determine whether collateral artery development is impaired in spontaneously hypertensive (SHR) relative to normotensive (WKY) rats.
  
  
  METHODS
  Sequential mesenteric arteries were ligated to create a collateral pathway responsible for the perfusion of approximately 50 first-order arterioles. Collateral development was assessed by measurement of in vivo arterial diameter before and 1 week after ligation. Histological and morphometric measurements were made from cross-sectional preparations of these arteries to evaluate intimal and medial cell numbers and medial area. eNOS expression was evaluated with Western blotting.
  
  
  RESULTS
  One week after arterial ligation, collateral diameter was increased more in WKY than SHR both absolutely (137 +/- 9.1 versus 99 +/- 8.6 microm) and relative to same-animal controls (38 +/- 5.5% versus 13 +/- 7.1%). At the time of model creation, blood flow was elevated to comparable levels in both WKY and SHR, and wall shear rate in the SHR collateral was greater than both the SHR control and WKY collateral arteries. Endothelial cell number in arterial cross-section was increased in collaterals by 80% in WKY and only 22% in the SHR. eNOS expression was increased in the WKY (128%) but not in the SHR collateral.
  
  
  CONCLUSIONS
  For equivalent arterial occlusion, the data demonstrate that collateral development is suppressed in the SHR as indicated by luminal expansion. This impairment of luminal expansion is associated with a decreased endothelial proliferation and the lack of an increase in eNOS expression.
authors.affiliation: Department of Surgery, Indiana University Medical Center, Indianapolis, IN 46202-2879, USA.
authors.forename: Jay L
authors.initials: JL
authors.lastname: Tuttle
authors.forename: Bridget M
authors.initials: BM
authors.lastname: Sanders
authors.forename: Harold M
authors.initials: HM
authors.lastname: Burkhart
authors.forename: Steven W
authors.initials: SW
authors.lastname: Fath
authors.forename: Kimberly A
authors.initials: KA
authors.lastname: Kerr
authors.forename: William C
authors.initials: WC
authors.lastname: Watson
authors.forename: B Paul
authors.initials: BP
authors.lastname: Herring
authors.forename: Michael C
authors.initials: MC
authors.lastname: Dalsing
authors.forename: Joseph L
authors.initials: JL
authors.lastname: Unthank
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000473:pathology / Q000503:physiopathology; D001158:Arteries / Q000254:growth & development*; D002455:Cell Division; D003097:Collateral Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000473:pathology; D006439:Hemodynamics; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D008638:Mesenteric Arteries; D019001:Nitric Oxide Synthase / Q000032:analysis / Q000096:biosynthesis; D052250:Nitric Oxide Synthase Type III; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY
chemical_list: D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat