Unger W G, Terenghi G, Ghatei M A, Ennis K W, Butler J M, Zhang S Q, Too H P, Polak J M, Bloom S R
Department of Visual Science, Institute of Ophthalmology, London.
J Ocul Pharmacol. 1985 Summer;1(2):189-99. doi: 10.1089/jop.1985.1.189.
Calcitonin gene-related polypeptide (CGRP) has been localised immunochemically within the rat and guinea pig anterior uvea to nerve fibres of trigeminal origin. As with substance P (1-3) the level of CGRP in the iris-ciliary body is depleted after thermal damage to the Gasserian ganglion and elevated in chronically sympathectically denervated eyes. Unlike substance P, a potent pupillary constrictor (4,5), CGRP has no notable miotic action, but does, however, cause an elevation of the intraocular pressure (IOP) accompanied by disruption of the blood-aqueous barrier. It is proposed that the diverse actions of these two sensory neuropeptides conjointly mediate the antidromic ocular injury response.
降钙素基因相关肽(CGRP)已通过免疫化学方法在大鼠和豚鼠眼前葡萄膜内定位到三叉神经起源的神经纤维。与P物质(1 - 3)一样,热损伤三叉神经节会使虹膜睫状体中的CGRP水平降低,而在长期交感神经去神经支配的眼睛中CGRP水平升高。与强力瞳孔收缩剂P物质不同(4,5),CGRP没有明显的缩瞳作用,但会导致眼压升高并伴有血-房水屏障破坏。有人提出,这两种感觉神经肽的不同作用共同介导了逆行性眼损伤反应。