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Christophe Delaey, Koen Boussery, Johan Van de Voorde; A Retinal-Derived Relaxing Factor Mediates the Hypoxic Vasodilation of Retinal Arteries. Invest. Ophthalmol. Vis. Sci. 2000;41(11):3555-3560.
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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)F2α (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 PGF2α. 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 PGF2α-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
PGF2α or 120 mM K+, whereas hypoxia induced
relaxation of the retinal artery contracted with PGF2α 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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