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A Retinal-Derived Relaxing Factor Mediates the Hypoxic Vasodilation of Retinal Arteries

From the Department of Physiology and Pathophysiology, Ghent University, Belgium.

PURPOSE. To investigate the mechanisms involved in hypoxic vasodilation using 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)F₂ (30 µM) or 120 mM K⁺. Hypoxia was induced by replacement of O₂ by N₂ 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 PGF₂. Preparations without retinal tissue were not affected by the change in oxygenation. When the retinal arteries were contracted with 120 mM K⁺, hypoxia no longer induced relaxation of the preparation with adherent retinal tissue. The presence of an NO-synthase inhibitor (L-NA, 0.1 mM), a cyclooxygenase inhibitor (indomethacin, 50 µM), or an adenosine receptor antagonist (8-sulfophenyltheophylline, 1 mM) did not affect hypoxic vasodilation. Excitatory amino acids and lactate had no or only a limited effect on the PGF₂-induced contraction and are therefore unlikely mediators of hypoxic vasodilation. HCl (10 mM) reduced the pH to 6.1 ± 0.08 (n = 4) and induced a pronounced but transient relaxation of the retinal artery contracted with PGF₂ or 120 mM K⁺, whereas hypoxia induced relaxation of the retinal artery contracted with PGF₂ 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, excitatory amino acids lactate or changes in pH seem to be involved in this hypoxic response.

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