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J. Carnes, K.R. M. Russell; Morphine–Induced Nitric Oxide Production in Isolated, Iris–Ciliary Bodies . Invest. Ophthalmol. Vis. Sci. 2006;47(13):428.
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We have recently shown that nitric oxide plays a role in morphine–induced reduction of intraocular pressure and pupil diameter in the New Zealand white rabbit (NZW). The present study is designed to determine the effect of morphine on nitric oxide production in the isolated, iris–ciliary body (ICB) of the NZW rabbit.
Iris–ciliary bodies obtained from normal rabbits were utilized in these experiments. In some experiments, ICB samples were treated with morphine (1, 10 and 100 µM) for 1 hour and later examined for changes in NO levels using a NO detection kit. In other experiments, tissue samples were pretreated with naloxone (non–selective opioid receptor antagonist) or L–NAME (non–selective NO synthase inhibitor) for 30 minutes, followed by treatment with morphine (10 uM).
Morphine caused a concentration–dependent increase in the release of NO from ICBs. Levels of NO detected in the incubation medium of ICB samples increased from 1.89 ± 0.26 (vehicle treated) to 4.84 ± 0.53 µM/mg protein (morphine treated; 10 µM). Morphine–stimulated release of NO was significantly inhibited in tissues pretreated with naloxone (10 µM) or L–NAME (100 µM).
Morphine–stimulated release of NO from the ICB is an opioid receptor–mediated effect. Results obtained from this study suggest that morphine–mediated regulation of IOP and pupil diameter is associated with increased production of NO in the iris–ciliary body.
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