Purchase this article with an account.
Sidse Kringelholt, Ulf Simonsen, Toke Bek; Dorzolamide-induced Vasorelaxation of Porcine Ciliary Arteries is Mediated by Nitric Oxide. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6857.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Carbonic anhydrase inhibitors (CAIs) are known to lower the intraocular pressure in glaucoma by reducing aqueous humor production. However, it is possible that other mechanisms, such as the regulation of blood flow to the ciliary body, are involved in the pressure lowering effect. This effect might be mediated by different transmitters including nitrogen oxide (NO).
The intraocular part of porcine ciliary arteries was isolated and mounted in a wire myograph system for isometric tension recordings.The effect of the CAI dorzolamide was tested on the tone of uveal arteries with and without endothelium, and in the presence or absence of the NO synthesis inhibitor L-NAME.
Dorzolamide induced a significant concentration-dependent relaxation of ciliary arteries. Removal of the endothelium and NO-inhibition significantly reduced dorzolamide-induced vasorelaxation (p<0.05, Student’s unpaired t-test).
Dorzolamide-induced vasorelaxation of ciliary arteries is mediated by endothelial nitric oxide. Several mechanisms may be responsible for the drugs beneficial effects in glaucoma, both including regulation of aqueous humor production and modulation of vascular tone.
This PDF is available to Subscribers Only