三磷肌醇、环磷酸腺苷对视网膜色素上皮功能影响的研究进展

Effect of Inositol Triphosphate,Cyclic Adenylate Monophosphate on Retinal Pigment Epithelial Cell Function

视网膜色素上皮（ｒｅｔｉｎａｌｐｉｇｍｅｎｔｅｐｉｔｈｅｌｉｕｍ，ＲＰＥ）胞膜上具有特异性受体，能辨认视细胞外节膜盘（ｒｏｄｏｕｔｅｒｓｅｇｍｅｎｔ，ＲＯＳ）上的特异性配体，受体与配体相互作用，ＲＰＥ细胞内三磷肌醇（ｉｎｏｓｉｔｏｌｔｒｉｐｈｏｓｐｈａｔｅ，ＩＰ３）的水平增高，可促使ＲＰＥ对ＲＯＳ的吞噬。另外，ＲＰＥ胞膜上的毒蕈碱受体与其激动剂作用后也可促使ＲＰＥ细胞内ＩＰ３的增高及对ＲＯＳ吞噬的增强。环磷酸腺苷（ｃｙｃｌｉｃａｄｅｎｙｌａｔｅｍｏｎｏｐｈｏｓｐｈａｔｅ，ｃＡＭＰ）则作用相反，ＲＰＥ细胞膜上存在β２肾上腺素能受体，其受体激动剂可刺激ＲＰＥ细胞内ｃＡＭＰ浓度的迅速升高，抑制ＲＰＥ的吞噬功能。ＩＰ３和ｃＡＭＰ之间是否有拮抗作用目前尚不清楚。ｃＡＭＰ还抑制ＲＰＥ细胞的趋化、迁移、和增殖，其机制不明。另外，ｃＡＭＰ通过促进ＲＰＥ胞膜上ＮＡ＋－Ｋ＋－ＡＴＰ酶的活性及抑制ＣＬ－由视网膜向脉络膜的转运而抑制视网膜下液的转运。

There are special receptors on the retinal pigment epithelial(RPE) cell membrane.When these receptors act with the adjacent rod outer segment (ROS),the level of inositol triphosphate(IP3) in RPE increases,which can enhance the ROS phagocytosis by RPE.In addition,when muscarinic receptors on the RPE cell membrane act with their ligands,IP3 increases and phagocytosis is enhanced similarly.Whereas,cyclic adenylate monophosphate(cAMP) has the opposite effect.The ligands of β2 epinephrine receptors acting with these receptors on the RPE cell membrane can increase the cAMP level in RPE rapidly,and phagocytosis by RPE is inhibited by cAMP.It is not known whether IP3 has antagonism with cAMP.cAMP also can inhibit the chemotaxis,migration and proliferation of RPE,but the mechanism is not known.cAMP can promote the activity of Na+-K+-ATPase on RPE apical membranes and inhibit CL- transport from retina to choroid,so cAMP can inhibit the transport of subretinal fluid.