Department of Pharmacology, Faculty of Pharmacy, Istanbul University, Istanbul, Turkey.
Microvasc Res. 2011 May;81(3):295-302. doi: 10.1016/j.mvr.2011.02.007. Epub 2011 Mar 5.
Retinal relaxing factor (RRF) is suggested to be released from the retina and to contribute in the maintenance of retinal arterial tone. Herein, we aimed to clarify the effects of retinal tissue in isolated bovine retinal arteries in comparison with choroidal tissue and to evaluate the possible role of endothelium and potassium channels. In parallel, the effects of palmitic acid methyl ester (PAME), a putative vasodilator proposed to be released from the retina, was also examined. A piece of bovine retinal or choroidal tissue was placed within a close proximity on top of retinal arteries mounted in a wire myograph and precontracted with noradrenaline, prostaglandin F(2α), endothelin-1, thromboxane A(2) mimetic, U46619 or potassium (K(+)). To elucidate possible mechanisms in the effects of retinal tissue, retinal arteries were either deendothelized or incubated with inhibitors of endothelial vasodilators, i.e. nitric oxide (NO) and prostaglandins, or K(+) channels. Unlike the choroid, retinal tissue produced rapid, biphasic and complete relaxations in isolated bovine retinal arteries precontracted with various spasmogens acting on distinct receptors. Endothelium removal or preincubation of retinal arteries with inhibitors of NO synthase; L-NOARG (10(-4)M), guanylate cyclase; ODQ (10(-5)M) and cyclooxygenase; indomethacin (10(-5)M), did not cause a significant difference in the relaxation profile. Additionally, retinal relaxations remained unchanged in the presence of respective inhibitors of ATP-sensitive (K(ATP)) (glibenclamide, 10(-5)M), voltage-dependent (K(V)) (4-aminopyridine, 2×10(-3)M), and calcium-activated (K(Ca)) (tetraethylammonium 10mM; charybdotoxin, 10(-7)M; and apamin, 5×10(-7)M) K(+) channels. Thus, our results provide novel evidence regarding the biphasic relaxing profile of RRF in the retinal artery which was unrelated to endothelium and K(+) channels (K(ATP), K(V) and K(Ca)). Interestingly, PAME (10(-14)-10(-5)M) did not provoke a relaxation in bovine retinal artery suggesting no association with RRF.
视网膜松弛因子 (RRF) 被认为是从视网膜中释放出来的，并有助于维持视网膜动脉的张力。在此，我们旨在阐明与脉络膜组织相比，牛视网膜组织对分离的牛视网膜动脉的作用，并评估内皮细胞和钾通道的可能作用。同时，还研究了棕榈酸甲酯 (PAME) 的作用，PAME 是一种被认为从视网膜释放的潜在血管扩张剂。将牛视网膜或脉络膜组织的一小片放置在安装在线性肌动描记器中的视网膜动脉上方，使其与去甲肾上腺素、前列腺素 F(2α)、内皮素-1、血栓烷 A(2) 模拟物、U46619 或钾 (K+) 预收缩。为了阐明视网膜组织作用的可能机制，将视网膜动脉去内皮化或用内皮血管扩张剂的抑制剂孵育，即一氧化氮 (NO) 和前列腺素，或 K+通道。与脉络膜不同，视网膜组织在各种作用于不同受体的收缩剂预收缩的分离的牛视网膜动脉中产生快速、双相和完全的松弛。去除内皮细胞或用 NO 合酶抑制剂；L-NOARG（10(-4)M）、鸟苷酸环化酶；ODQ（10(-5)M）和环氧化酶；吲哚美辛（10(-5)M）预孵育视网膜动脉不会导致松弛谱的显著差异。此外，在存在相应的 ATP 敏感性 (K(ATP))（格列本脲，10(-5)M）、电压依赖性 (K(V))（4-氨基吡啶，2×10(-3)M）和钙激活 (K(Ca))（四乙铵 10mM；蟾毒肽，10(-7)M；和阿帕米，5×10(-7)M）K+通道抑制剂的情况下，视网膜松弛仍然不变。因此，我们的结果提供了关于 RRF 在视网膜动脉中的双相松弛特征的新证据，这与内皮细胞和 K+通道 (K(ATP)、K(V) 和 K(Ca))无关。有趣的是，PAME（10(-14)-10(-5)M）没有引起牛视网膜动脉的松弛，这表明与 RRF 无关。
