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.