Delaey C, Van de Voorde J
Department of General Physiology and Human Physiology and Pathophysiology, University of Gent, Belgium.
Circ Res. 1998 Oct 5;83(7):714-20. doi: 10.1161/01.res.83.7.714.
The present study provides evidence that retinal tissue may profoundly influence the retinal arterial smooth muscle cell tone by releasing an unknown retinal relaxing factor. Isolated bovine retinal arteries with and without adhering retinal tissue were mounted in a wire myograph for isometric tension recordings. The maximal contraction induced by prostaglandin F2alpha was 0.95+/-0.7 mN (n=6) in the presence and 5.15+/-0.76 mN (n=6) in the absence of adhering retinal tissue. The contractions induced by U-46619, serotonin, and endothelin-1 were similarly blocked in the presence of retinal tissue. The K+ 120 mmol/L-induced contraction was not significantly affected (2.8+/-0.7 mN, n=6, in the presence and 3. 6+/-0.7 mN, n=6, in the absence of retinal tissue). Placing a piece of bovine retinal tissue in the proximity of a contracted (ie, with prostaglandin F2alpha) retinal artery induced a complete relaxation of the retinal vessel, suggesting the involvement of a diffusible chemical vasorelaxant. Also porcine, canine, and ovine retinal tissue completely relaxed the contracted (with prostaglandin F2alpha) bovine retinal artery. Other smooth muscle preparations, including rat mesenteric and renal arteries and rat main bronchi, also relaxed with the application of a piece of bovine retinal tissue. Incubation of bovine retinas in a Krebs-Ringer bicarbonate solution yielded a solution that relaxed isolated precontracted bovine retinal arteries, confirming the involvement of a diffusible chemical messenger. Hexane extraction, heating the solution to 70 degrees C, or treatment with trypsin did not alter the relaxing properties of the incubation solution. The characteristics of the retinal relaxing factor do not correspond with those of nitric oxide, prostanoids, adenosine, acetylcholine, or any other of the known vasoactive neurotransmitters released from the retina. Our results suggest that retinal arterial tone is controlled by a diffusible, hydrophilic, and heat-stable relaxing factor that does not correspond with a known vasoactive molecule formed within the retina.
本研究提供了证据表明，视网膜组织可能通过释放一种未知的视网膜舒张因子深刻影响视网膜动脉平滑肌细胞的张力。将带有和不带有附着视网膜组织的离体牛视网膜动脉安装在线肌张力描记仪中进行等长张力记录。在有附着视网膜组织时，前列腺素F2α诱导的最大收缩为0.95±0.7 mN（n = 6），在无附着视网膜组织时为5.15±0.76 mN（n = 6）。在有视网膜组织存在时，U - 46619、5 - 羟色胺和内皮素 - 1诱导的收缩同样受到抑制。120 mmol/L钾离子诱导的收缩没有受到显著影响（有视网膜组织时为2.8±0.7 mN，n = 6；无视网膜组织时为3.6±0.7 mN，n = 6）。将一片牛视网膜组织放置在收缩的（即由前列腺素F2α诱导收缩）视网膜动脉附近，可使视网膜血管完全舒张，提示存在一种可扩散的化学血管舒张剂。猪、犬和羊的视网膜组织也能使收缩的（由前列腺素F2α诱导）牛视网膜动脉完全舒张。其他平滑肌标本，包括大鼠肠系膜动脉、肾动脉和大鼠主支气管，在应用一片牛视网膜组织后也会舒张。将牛视网膜在 Krebs - Ringer 碳酸氢盐溶液中孵育，得到的溶液能使离体预收缩的牛视网膜动脉舒张，证实存在一种可扩散的化学信使。己烷萃取、将溶液加热至70摄氏度或用胰蛋白酶处理均未改变孵育溶液的舒张特性。视网膜舒张因子的特性与一氧化氮、前列腺素、腺苷、乙酰胆碱或从视网膜释放的任何其他已知血管活性神经递质的特性均不相符。我们的结果表明，视网膜动脉张力受一种可扩散、亲水性且热稳定的舒张因子控制，该因子与视网膜内形成的已知血管活性分子不同。
