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on
retinal vessels
1 Departments of Pediatrics,
Using a video-imaging technique, we
characterized the effects of 8-isoprostaglandin
F2
(8-iso-PGF2) on retinal
vasculature from piglets.
8-Iso-PGF2 potently contracted
(EC50 = 5.9 ± 0.5 nM) retinal
vessels. These effects were completely antagonized by the
cyclooxygenase inhibitor indomethacin, the thromboxane synthase blocker
CGS-12970, the thromboxane receptor antagonist L-670596, and the
putative inhibitor of the non-voltage-dependent receptor-operated
Ca2+ pathway SKF-96365;
constrictor effects of
8-iso-PGF2 were also partly
attenuated by the ETA-receptor
blocker BQ-123 and an inhibitor of endothelin-converting enzyme,
phosphoramidon, but was negligibly affected by the L-type voltage-gated
Ca2+ channel blocker nifedipine.
Correspondingly, 8-iso-PGF2 elicited endothelin release from retinal preparations, which was markedly reduced by SKF-96365.
8-Iso-PGF2 also increased thromboxane production in the retina and cultured endothelial cells,
but not on retinovascular smooth muscle cells; these effects of
8-iso-PGF2 were blocked by
indomethacin, CGS-12970, SKF-96365, and EGTA, but not by nifedipine.
8-Iso-PGF2 also increased Ca2+ transients in retinal
endothelial cells, which were inhibited by SKF-96365 and EGTA, but not
by nifedipine, whereas in smooth muscle cells U-46619, but not
8-iso-PGF2, stimulated a rise in Ca2+ transients. Finally,
H2O2 + FeCl2 (in vitro) and anoxia
followed by reoxygenation (in vivo) stimulated formation of
8-iso-PGF2 in the retina. In
conclusion, 8-iso-PGF2-induced
retinal vasoconstriction is mediated by cyclooxygenase-generated
formation of thromboxane and, to a lesser extent, by endothelin after
Ca2+ entry into cells, possibly
through receptor-operated channels. Retinal vasoconstriction to
8-isoprostanes might play a role in the genesis of ischemic
retinopathies.
peroxidation; calcium influx; cyclooxygenase; thromboxane; endothelin
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