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. 1995 Nov;116(5):2447–2450. doi: 10.1111/j.1476-5381.1995.tb15094.x

Role of nitric oxide (NO) in ocular inflammation.

Z Y Wang 1, R Håkanson 1
PMCID: PMC1909062  PMID: 8581283

Abstract

1. The actions of nitric oxide (NO) have been investigated in the rabbit eye, with particular emphasis on the relationship between NO and C-fibres and on those effects of NO that may be of importance in the inflammatory response to C-fibre stimulation. 2. The NO synthase inhibitor, NG-nitro-L-arginine (L-NAME; 10-200 mg kg-1), but not the inactive analogue D-NAME (200 mg kg-1), was found to block the inflammatory response induced by infrared irradiation of the iris in a dose-dependent manner. The inhibitory effects of L-NAME (200 mg kg-1) were partially reversed by L-arginine (500 mg kg-1), but not by D-arginine (500 mg kg-1). 3. L-NAME (200 mg kg-1) virtually abolished the ocular effects of intravitreal injection of calcitonin gene-related peptide (CGRP) (0.3 nmol). 4. The concentration of CGRP in aqueous humour from untreated rabbit eyes was 0.1 +/- 0.001 nmol l-1. Irradiation of the iris raised the CGRP concentration to 8.9 +/- 1.5 nmol l-1. L-NAME (200 mg kg-1) greatly suppressed the irradiation-evoked release of CGRP, the concentration in the aqueous humour being 1.2 +/- 0.2 nmol l-1 (P < 0.001). L-Arginine reversed the L-NAME-induced inhibition of release of CGRP, the concentration of CGRP in the aqueous humour being 9.7 +/- 0.6 nmol l-1. 5. In addition, a NO donor, sodium nitroprusside (0.9 mumol), was found to raise the concentration of CGRP in the aqueous humour (14.8 +/- 0.8 nmol l-1) and to induce symptoms of ocular inflammation. The elevation in concentration of CGRP induced by sodium nitroprusside was not affected by L-NAME (200 mg kg-1) (14.5 +/- 1.2 nmol l-1). Ocular responses were not inhibited by L-NAME. 6. Our findings suggest that NO plays an important role in ocular inflammation by activating C-fibres (directly or indirectly) and by mediating CGRP-induced responses.

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Selected References

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