title: Biomechanics of resistance artery wall remodeling in angiotensin-II hypertension and subsequent recovery.
abstract: OBJECTIVE
  To identify the relationship between systemic and local hemodynamics, as well as segmental biomechanical properties in a musculocutaneous resistance artery during angiotensin-II hypertension and its recovery.
  
  
  METHODS
  Rats were infused with angiotensin-II using implanted osmotic minipumps (ALZET 2ML4, 150 ng/kg/min) for 4 weeks. Measurements were made either immediately following infusion or after an additional 4-week recovery period. Parallel controls were created. Segmental geometry and blood flow were determined in vivo on microsurgically exposed segments of the saphenous arterial branch (350 mum). Pressure-radius plots of excised cylindrical segments were recorded by pressure arteriography.
  
  
  RESULTS
  Eutrophic hypertensive wall remodeling developed, with reduced passive radius, increased wall thickness, elevated low-stress elastic modulus, reduced norepinephrine contraction, and reduced endothelium-mediated dilation. Relaxed wall geometry fully healed in 4 weeks of recovery, but an increased contractility and a reduced in vivo lumen persisted. Regional hemodynamic resistance correlated positively with systemic arterial pressure and wall thickness in vivo, and negatively with in vivo lumen size throughout these studies.
  
  
  CONCLUSIONS
  A partial recovery of the biomechanical parameters was found. Healing of eutrophic hypertensive remodeling of the resistance artery wall is a complex biomechanical process, not a simple reversal of the original pathological sequel.
authors.affiliation: Department of Clinical Research and Human Physiology, Semmelweis University, Budapest, Hungary. nadasy@elet2.sote.hu
authors.forename: György L
authors.initials: GL
authors.lastname: Nádasy
authors.forename: Szabolcs
authors.initials: S
authors.lastname: Várbíró
authors.forename: Mária
authors.initials: M
authors.lastname: Szekeres
authors.forename: Adrienn
authors.initials: A
authors.lastname: Kocsis
authors.forename: Béla
authors.initials: B
authors.lastname: Székács
authors.forename: Emil
authors.initials: E
authors.lastname: Monos
authors.forename: Márk
authors.initials: M
authors.lastname: Kollai
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001696:Biomechanical Phenomena; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002339:Carotid Arteries / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D004548:Elasticity; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D006977:Hypertension, Renal / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000502:physiology*; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D009638:Norepinephrine