title: Angiotensin II contributes to the increased baseline leg vascular resistance in spinal cord-injured individuals.
abstract: OBJECTIVE
  Spinal cord-injured (SCI) individuals demonstrate an increased baseline leg vascular resistance (LVR). In addition, despite the lack of sympathetic control, an increase in LVR is observed during orthostatic challenges. On the basis of the vasoconstrictive characteristics of angiotensin II, we examined the hypothesis that angiotensin II contributes to the LVR at baseline and during head-up tilt (HUT) in SCI individuals.
  
  
  METHODS
  Supine baseline leg and forearm blood flow were measured using venous occlusion plethysmography and leg blood flow during 30° HUT using duplex ultrasound. Measurements were performed before and 4 h after an angiotensin II antagonist (irbesartan, 150 mg) administered in eight SCI individuals and eight age-matched and sex-matched able-bodied controls. Vascular resistance was calculated as the arterial-venous pressure gradient divided by blood flow.
  
  
  RESULTS
  Angiotensin II blockade significantly decreased baseline LVR in SCI individuals (P = 0.02) but not in controls, whereas no changes in forearm vascular resistance were found in both groups. Angiotensin II blockade did not alter the increase in LVR during HUT in SCI individuals nor in controls.
  
  
  CONCLUSIONS
  Our results indicate that angiotensin II contributes to the increased baseline LVR in SCI individuals. As angiotensin II does not contribute to forearm vascular resistance, the contribution to LVR may relate to the extreme inactivity of the legs in SCI individuals. Angiotensin II does not contribute to the increase in LVR during HUT in SCI individuals nor in controls.
authors.affiliation: aDepartment of Physiology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
authors.forename: Jan T
authors.initials: JT
authors.lastname: Groothuis
authors.forename: Dick H J
authors.initials: DH
authors.lastname: Thijssen
authors.forename: Gerard A
authors.initials: GA
authors.lastname: Rongen
authors.forename: Jaap
authors.initials: J
authors.lastname: Deinum
authors.forename: A H Jan
authors.initials: AH
authors.lastname: Danser
authors.forename: Alexander C H
authors.initials: AC
authors.lastname: Geurts
authors.forename: Paul
authors.initials: P
authors.lastname: Smits
authors.forename: Maria T E
authors.initials: MT
authors.lastname: Hopman
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000502:physiology*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D001713:Biphenyl Compounds / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D016022:Case-Control Studies; D006801:Humans; D000077405:Irbesartan; D007866:Leg / Q000098:blood supply*; D008297:Male; D008875:Middle Aged; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D016683:Supine Position / Q000502:physiology; D013777:Tetrazoles / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D001713:Biphenyl Compounds; D013777:Tetrazoles; D000804:Angiotensin II; D000077405:Irbesartan