Abstract
Abstract: :
Purpose: Noladin ether is an endogenous cannabinoid agonist selective for CB1 receptor. The lowering intraocular pressure (IOP)–lowering effects of Noladin ether has been shown in previous studies but the mechanisms for Noladin ether–induced IOP–lowering effects are unknown. The objective of this study was to investigate the effect of Noladin ether on aqueous humor outflow facility and to test whether its action is CB1 receptor–mediated. Methods: Porcine anterior segment perfused organ culture model was used to measure the effects of Noladin ether on aqueous humor outflow facility. Anterior segment explants were mounted on perfusion chamber and perfused with culture medium at constant pressure of 7.35mmHg. After the outflow facility had been stabilized, Noladin ether was administrated to the perfusion medium and the outflow facility was observed for 5 hours. Results:Noladin ether produced a significant enhancement of outflow facility. This effect was dose–dependent with a maximum effect occurring at 30nM of Noladin ether. In addition, the effect of 30nM of Noladin ether was completely blocked by 300nM of SR141716A, a selective CB1 receptor antagonist. Conclusions: The data obtained from this study demonstrate that Noladin ether increases aqueous humor outflow facility and that its effect is mediated through the CB1 cannabinoid receptor.
Keywords: trabecular meshwork • intraocular pressure • aqueous