title: Dilatation in the femoral vascular bed does not cause retrograde relaxation of the iliac artery in the anaesthetized pig.
abstract: OBJECTIVE
  We tested the hypothesis that dilatation of a feeding artery may be elicited by transmission of a signal through the tissue of the arterial wall from a vasodilated peripheral vascular bed.
  
  
  METHODS
  In eight pentobarbital anaesthetized pigs, acetylcholine (ACh, an endothelium-dependent vasodilator) was injected intra-arterially above (upstream) and below (downstream) a test segment of the left iliac artery, the diameter of which was measured continuously by sonomicrometry.
  
  
  RESULTS
  Under control conditions, ACh injections upstream and downstream of the test segment caused dilatation. Downstream injection dilated the peripheral arterioles, resulting in increased blood flow and proximal dilatation. This is a shear stress, nitric oxide (NO)-dependent response. The experiment was then repeated after applying a stenosis to prevent the increased flow caused by downstream injection of ACh; the stenosis was placed either above the site of diameter measurement to allow retrograde conduction, or below that site to prevent distally injected ACh reaching the measurement site. Under these conditions, downstream injection of ACh had a minimal effect on the shear stress of the test segment with no increase in test segment diameter. This was not due to endothelial damage or dysfunction as injection of ACh upstream still caused a large increase in test segment diameter.
  
  
  CONCLUSIONS
  Our results indicate that dilatation of the feeding artery of a vasodilated bed is caused by increased shear stress within the feeding artery and not via a signal transmitted through the arterial wall from below.
authors.affiliation: Department of Physiology, University College Cork, Cork, Ireland. f.markos@ucc.ie
authors.forename: F
authors.initials: F
authors.lastname: Markos
authors.forename: T
authors.initials: T
authors.lastname: Ruane-O'Hora
authors.forename: H M
authors.initials: HM
authors.lastname: Snow
authors.forename: R
authors.initials: R
authors.lastname: Kelly
authors.forename: C
authors.initials: C
authors.lastname: Wainwright
authors.forename: K
authors.initials: K
authors.lastname: Skene
authors.forename: A J
authors.initials: AJ
authors.lastname: Drake-Holland
authors.forename: M I M
authors.initials: MI
authors.lastname: Noble
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000768:Anesthesia, General; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D005269:Femur / Q000098:blood supply*; D007083:Iliac Artery / Q000502:physiology*; D012039:Regional Blood Flow / Q000187:drug effects; D013314:Stress, Mechanical; D034421:Sus scrofa; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D000109:Acetylcholine