title: Relaxation of porcine retinal arterioles during acute hypoxia in vitro depends on prostaglandin and NO synthesis in the perivascular retina.
abstract: OBJECTIVE
  Disturbances in retinal oxygenation influence retinal function, but are also accompanied by changes in the tone of retinal arterioles. However, the mechanisms underlying these tone changes have not been studied in detail.
  
  
  METHODS
  Porcine retinal arterioles were mounted in a wire myograph, and the vasoactive effects of hypoxia and hyperoxia were studied before and after removal of the perivascular retinal tissue. Subsequently, the experiments were repeated in the presence of antagonists to prostaglandins, nitric oxide (NO), adenosine and glutamate.
  
  
  RESULTS
  Hypoxia induced a significant concentration-dependent relaxation of U46619-contracted retinal arterioles which depended on the presence of the perivascular retinal tissue. The relaxation was significantly reduced by inhibiting the synthesis of prostaglandins and NO simultaneously. The recovery of vascular tone after hypoxia was incomplete, but increased to a normal level during the inhibition of prostaglandin synthesis. Hyperoxia induced a slight concentration-dependent contraction of retinal arterioles that was not affected by any of the antagonists used.
  
  
  CONCLUSIONS
  Hypoxia-induced relaxation of porcine retinal arterioles in vitro depends on prostaglandins and NO and the presence of perivascular retinal tissue, whereas recovery of tone after hypoxia depends on the action of prostaglandins. Clinical intervention studies of these effects may help treating retinal diseases where disturbances in tissue oxygenation are involved in the disease pathogenesis.
authors.affiliation: Department of Ophthalmology, Aarhus University Hospital, DK-8000 Aarhus C, Denmark. sidse@kringelholt.dk
authors.forename: Sidse
authors.initials: S
authors.lastname: Kringelholt
authors.forename: Kim
authors.initials: K
authors.lastname: Holmgaard
authors.forename: Toke
authors.initials: T
authors.lastname: Bek
mesh_terms: D000208:Acute Disease; D000241:Adenosine / Q000378:metabolism; D000818:Animals; D001160:Arterioles / Q000378:metabolism / Q000502:physiology*; D018698:Glutamic Acid / Q000378:metabolism; D018496:Hyperoxia / Q000378:metabolism / Q000503:physiopathology; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D009213:Myography; D009569:Nitric Oxide / Q000096:biosynthesis* / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D011453:Prostaglandins / Q000378:metabolism*; D012171:Retinal Vessels / Q000378:metabolism / Q000502:physiology*; D013552:Swine; D014664:Vasodilation / Q000502:physiology*
chemical_list: D011453:Prostaglandins; D009569:Nitric Oxide; D018698:Glutamic Acid; D000241:Adenosine; D010100:Oxygen