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Z.-H. Song, Z. Xiao, W. Wang, Y. Njie; CB1 and CB2 Agonists Increase Uveoscleral Outflow. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1478.
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To study the effects of noladin ether, a cannabinoid agonist selective for CB1 receptor, and JWH015, a cannabinoid agonist selective for CB2 receptor, on aqueous humor outflow via the uveoscleral pathway.
The effects of noladin ether and JWH015 on aqueous humor outflow facility via the uveoscleral pathway were measured using an in vitro single-level constant pressure perfusion technique. After measurement of total outflow, the episcleral vessels were blocked with ethyl cyanoacrylate to eliminate outflow through the conventional (trabecular meshwork) pathway. Following stabilization for 3 hours, different concentrations of either noladin ether or JWH015 were administered to the perfused eyes and the outflow was monitored for 5 hours. To investigate whether CB1 and CB2 cannabinoid receptors are involved in the uveoscleral outflow effects induced by CB1 agonist noladin ether and CB2 agonist JWH015, respectively, CB1 antagonist SR141716A and CB2 antagonist SR144528 were administered to the perfused eyes 30 minutes prior to the application of their respective agonists.
Administration of neither 30 nM noladin ether nor 30 nM JWH015 caused a significant change in uveoscleral outflow. However, both 300 nM noladin ether and 300 nM JWH015 led to a significant increase in uveoscleral outflow. Pretreatment with 1 µM of SR141716A produced a partial antagonism on the noladin ether-induced enhancement of uveoscleral outflow. Likewise, pretreatment with 1 µM of SR144528 partially blocked the outflow-enhancing effects induced by JWH015.
The results from this study demonstrate that CB1 agonist noladin ether and CB2 agonist JWH015 increase uveoscleral outflow, and these effects are partially dependent of CB1 and CB2 cannabinoid receptors, respectively.
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