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Olga Kudryavtseva, Toke Bek; Ca2+ signaling in perivascular cells during PGE2-induced relaxation and PGF2α-induced contraction of porcine retinal arterioles in vitro . Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4418.
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© ARVO (1962-2015); The Authors (2016-present)
Recently, a novel population of perivascular cells (PVC) located immediately external to the vascular smooth muscle cells of the retinal arterioles has been identified. PVCs may contribute to agonist-induced modulation of retinal arterioles tone, and the purpose of the present study was to identify the source of Ca2+ recruitment in the perivascular cells during PGE2-induced relaxation and PGF2α-induced contraction of porcine retinal arterioles.
Porcine retinal arterioles with preserved perivascular retinal tissue were mounted in a confocal myograph and loaded with the Ca2+-sensitive fluorophore Oregon Green. After either pre-constriction with U46619 (10-6 M) followed by the addition of the relaxing prostaglandin PGE2 (10-5 M) or addition of the constricting prostaglandin PGF2α (10-5 M) arteriolar tone and fluorescence from PVCs were recorded simultaneously with and without the presence of Ca2+ channel blockers (ryanodine, nifedipine, LOE908, CPA, 2-APB).
The addition of PGE2 induced arteriolar relaxation and none of the Ca2+ channel blockers caused significant changes in this relaxation. Both PGE2 and PGF2α increased Ca2+ activity in the PVCs. CPA and 2-APB reduced the number of PVCs displaying Ca2+ activity after stimulation with both compounds, whereas ryanodine, nifedipine and LOE908 reduced calcium acitivity in PVCs stimulated with PGF2α.
PGE2 and PGF2α induce Ca2+ activity in perivascular cells of porcine retinal arterioles, and sarcoplasmic reticulum and inositol triphosphate receptors are important sources of this Ca2+ signal. A coupling between PGE2-induced relaxation and Ca2+ recruitment in perivascular retinal cells is uncertain.
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