Retina evokes biphasic relaxations in retinal artery unrelated to endothelium, KV, KATP, KCa channels and methyl palmitate

Constriction of porcine retinal arterioles induced by endothelin‐1 and the thromboxane analogue U46619 in vitro decreases with increasing vascular branching level

“…This is in accordance with the finding that porcine and bovine retinal arterioles with preserved perivascular retinal tissue produce a lower constrictive response after stimulation with vasoconstrictors than isolated retinal arterioles (Delaey & Van de Voorde 1998; Holmgaard et al. 2008; Takir et al. 2011), suggesting an inhibiting effect on the constriction from the perivascular retina.…”

“…1994) and from observations in rat and bovine tissue (Mori et al. 2011; Takir et al. 2011), but confirms previous studies on porcine retinal arterioles in the wire myographs (unpublished results).…”

Neuropeptide Y treatment induces retinal vasoconstriction and causes functional and histological retinal damage in a porcine ischaemia model

“…Indeed, reduction in retinal blood flow, but not choroidal blood flow, has been described in cats treated with intravitreal injection of another known vasoconstrictor, endothelin 1 (Granstam et al 1992;Pang & Clark 2010). The NPY-induced constriction in our study was less than one-third of the constriction seen with endothelin-1 in both ophthalmic and retinal arteries (Delaey & Van de Voorde 1998;Takır et al 2011;Blixt et al 2016), and the potential reduction in blood flow caused by exogenous NPY is probably not strong enough to induce significant ischaemia by itself. The NPY-induced constriction in our study was less than one-third of the constriction seen with endothelin-1 in both ophthalmic and retinal arteries (Delaey & Van de Voorde 1998;Takır et al 2011;Blixt et al 2016), and the potential reduction in blood flow caused by exogenous NPY is probably not strong enough to induce significant ischaemia by itself.…”

NaHS induces relaxation response in prostaglandin F2α precontracted bovine retinal arteries partially via Kv and Kir channels

“…The role of endothelial vasodilators in the relaxation response to NaHS in the retinal arteries were evaluated in the presence of the known inhibitors of NO synthase, guanylate cyclase or cyclooxygenase enzymes as well as following the removal of the endothelium (Takır et al, 2011). Thereby, incubation of the retinal arteries with L-NOARG (100 mM), ODQ (10 mM) or indomethacin (10 mM), respectively, for 20 min or the removal of the endothelium did not significantly modify the relaxation responses to NaHS (1mMe3 mM) (E max : in the presence of L-NOARG: 60.73 ± 7.62%; ODQ: 58.36 ± 6.51%; indomethacin: 60.66 ± 7.61% and deendothelized: 59.45 ± 3.37% vs. corresponding controls, n ¼ 7e10, p > 0.05) (Fig.…”

“…The probable role of different types of K þ channels in NaHS induced vasodilatation were tested by using the known inhibitors of K ATP , K v , K Ca þþ and K ir channels (Takır et al, 2011). Incubation of the retinal arteries for 20 min with K ATP channel inhibitor, glibenclamide (10 mM), non-specific K þ channel inhibitor, TEA (10 mM), SK Ca þþ channel inhibitor, apamin (300 nM) or the combination of IK Ca þþ /BK Ca þþ channel inhibitor, charybdotoxin (100 nM) with apamin (300 nM) did not modify the relaxation responses to NaHS (1mMe3 mM) (E max : in the presence of glibenclamide: 54.88 ± 9.82%, n ¼ 7, TEA: 57.49 ± 8.72%, n ¼ 6, apamin: 58.02 ± 11.60%, n ¼ 9 and charybdotoxin þ apamin: 47.29 ± 4.07%, n ¼ 6 vs. corresponding controls, p > 0.05) (Fig.…”