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Abstract #12560 Published in IGR 7-3
2-(1-Hexyn-1-yl)adenosine-induced intraocular hypertension is mediated via K+ channel opening through adenosine A2A receptor in rabbits
Konno T; Uchibori T; Nagai A; Kogi K; Nakahata NEuropean Journal of Pharmacology 2005; 518: 203-211
The present study was performed to clarify the mechanism of change in intraocular pressure by 2-(1-hexyn-1-yl)adenosine (2-H-Ado), a selective adenosine A2 receptor agonist, in rabbits. 2-H-Ado (0.1%, 50 μl)-induced ocular hypertension (Emax : 7.7 mmHg) was inhibited by an adenosine A2A receptor antagonist 1,3,7-trimethyl-8-(3-chlorostyryl)xanthine, ATP-sensitive K+ channel blocker glibenclamide or 5-hydroxydecanoic acid, but not by an adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine, an adenosine A2B receptor antagonist alloxazine or a cyclooxygenase inhibitor indomethacin. The outflow facility induced by 2-H-Ado seems to be independent of increase in intraocular pressure or ATP-sensitive K+ channel. In contrast, the recovery rate in intraocular pressure decreased by hypertonic saline was accelerated by 2-H-Ado, and this response was dependent on ATP-sensitive K+ channel. These results suggest that 2-H-Ado-induced ocular hypertension is mediated via K+ channel opening through adenosine A2A receptor, and this is probably due to aqueous formation, but independent of change in outflow facility or prostaglandin production.
Dr. T. Konno, Drug Research Section II, Fukushima Research Laboratories, Toa Eiyo Ltd., Iizaka, Fukushima 960-0280, Japan. konno.takashi@toaeiyo.co
Classification:
5 Experimental glaucoma; animal models
2.6.2 Outflow (Part of: 2 Anatomical structures in glaucoma > 2.6 Aqueous humor dynamics)
3.8 Pharmacology (Part of: 3 Laboratory methods)
