title: Pressure but not angiotensin II-induced increases in wall mass or tone influences static and dynamic aortic mechanics.
abstract: OBJECTIVE
  To distinguish between static (due to slow changes in pressure) and dynamic (due to pressure pulsatility) components of aortic compliance over a large pressure range in vivo and to examine the effects of increased vascular mass and smooth muscle tone on these components.
  
  
  METHODS
  Using ultrasound wall tracking, aortic lumen area-pressure curves were generated in anaesthetized rats over a broad range of pressures by altering blood volume. The compliance coefficient calculated at each mean pressure was considered the dynamic compliance at that pressure; the slope of the diastolic lumen area-pressure curve represents static compliance. Experiments were performed in control rats and rats treated with angiotensin II (ANG II) acutely (500 ng/kg per min intravenously) to modify vascular tone or chronically (250 ng/kg per min subcutaneously for 2 weeks) to modify vascular mass.
  
  
  RESULTS
  The dynamic compliance-pressure curve approximated a parabola. Maximal dynamic compliance (0.272+/-0.026 mm2/kPa in control rats) was achieved at near-normotensive pressure (+/-105 mm Hg). The diastolic lumen area-pressure curve showed an exponential relationship within a physiological range (30-130 mm Hg). ANG II-induced increases in aortic wall mass or smooth muscle tone did not modify the relationship between static or dynamic compliance and pressure.
  
  
  CONCLUSIONS
  These findings demonstrate that static and dynamic mechanics of the rat thoracic aorta depend differently on blood pressure. Static compliance increases slightly with pressure in a physiological range, while dynamic compliance is auto-regulated around normotensive pressures. Neither static nor dynamic compliance of the rat thoracic aorta are influenced by ANG II-induced increases in aortic wall mass or smooth muscle tone.
authors.affiliation: Department of Pharmacology, Cardiovascular Research Institute Maastricht, Universiteit Maastricht, The Netherlands. D.Ceiler@Farmaco.Unimaas.nl
authors.forename: D L
authors.initials: DL
authors.lastname: Ceiler
authors.forename: H J
authors.initials: HJ
authors.lastname: Nelissen-Vrancken
authors.forename: J F
authors.initials: JF
authors.lastname: Smits
authors.forename: J G
authors.initials: JG
authors.lastname: De Mey
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D003187:Compliance / Q000187:drug effects; D006984:Hypertrophy / Q000503:physiopathology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology*; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D000804:Angiotensin II