Outflow facility in the monkey eye: Effects of calcitonin gene-related peptide, cholecystokinin, galanin, substance P and capsaicin

Abstract

A study in cats has shown that intracameral injection of calcitonin gene-related peptide (CGRP) increases the outflow facility by four- to fivefold concomitant with a decrease in intra-ocular pressure (IOP). Since there are great differences in the anatomy of the aqueous outflow routes between cats and primates, we have examined the effects of CGRP in the cynomolgus monkey. The possible influence of the sensory neuropeptides cholecystokinin (CCK), galanin and substance P on the outflow facility and IOP were also investigated. Determinations were performed using a two-level constant-pressure procedure. At 40–60 min after intracameral injection of 3 μg CGRP the outflow facility was increased from 0·68±0·11 to 1·03±0·15 μl min −1 mmHg −1 in the CGRP-treated eyes, and from 0·71±0·12 to 0·79±0·10 μl min −1 mmHg −1 in the control eyes. The mean difference in increase was 0·27±0·06 μl min −1 mmHg −1 ( P < 0·01, n = 7). During the experiments there was a small rise in the IOP. CGRP at a dose of 3 μg caused a small rise in aqueous humor protein concentration. An attempt to release endogenous CGRP with capsaicin did not result in an increased outflow facility. Three micrograms each of CCK, galanin and substance P had no significant effect on either the outflow facility or the IOP. A miosis was observed in the experiments with CCK in agreement with previous findings. CCK seems thus to cause contraction of the pupillary sphincter but does not influence the ciliary muscle sufficiently to cause a facility effect in the monkey eye. Our results indicate that the effect of CGRP on the outflow facility in the monkey eye is much smaller than in cats, and that the other sensory neuropeptides tested have no clear effects on the conductance of the outflow routes.