A retinal-derived relaxing factor mediates the hypoxic vasodilation of retinal arteries

PURPOSE. To investigate the mechanisms involved in hypoxic vasodilation usi ng an in vitro setup. METHODS. Retinal arteries with and without retinal tissue were mounted on a wire myograph. The segments were contracted with prostaglandin (PG)F-2 alp ha (30 mu M) or 120 mM K+. Hypoxia was induced by replacement of O-2 by N-2 in the gas used to bubble the Krebs-Ringer bicarbonate organ bath solution . RESULTS. Hypoxia induced complete relaxation of preparations with adherent retinal tissue contracted with PGF(2 alpha). Preparations without retinal t issue were not affected by the change in oxygenation. When the retinal arte ries were contracted with 120 mM K+, hypoxia no longer induced relaxation o f the preparation with adherent retinal tissue. The presence of an NO-synth ase inhibitor (L-NA, 0.1 mM), a cyclooxygenase inhibitor (indomethacin, 50 mu M), or an adenosine receptor antagonist (8-sulfophenyltheophylline, 1 mM ) did not affect hypoxic vasodilation. Excitatory amino acids and lactate h ad no or only a limited effect on the PGF(2 alpha)-induced contraction and are therefore unlikely mediators of hypoxic vasodilation. HCl (10 mM) reduc ed the pH to 6.1 +/- 0.08 (n = 4) and induced a pronounced but transient re laxation of the retinal artery contracted with PGF(2 alpha) or 120 mM K+, w hereas hypoxia induced relaxation of the retinal artery contracted with PGF (2 alpha) only in the presence of adherent retinal tissue. CONCLUSIONS. Adherent retinal tissue mediates the hypoxic vasodilatation of bovine retinal arteries in vitro. Neither NO, prostanoids, adenosine, exci tatory amino acids lactate or changes in pH seem to be involved in this hyp oxic response.