2-(1-Hexyn-1-yl)adenosine-induced intraocular hypertension is mediated via K+ channel opening through adenosine A2A receptor in rabbits
| Autor: | Akihiko Nagai, Takehiro Uchibori, Takashi Konno, Kentaro Kogi, Norimichi Nakahata |
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| Rok vydání: | 2004 |
| Předmět: |
Male
medicine.medical_specialty Adenosine Potassium Channels Time Factors Adenosine A2 Receptor Agonists Receptor Adenosine A2A Adenosine A2A receptor Sodium Chloride Adenosine A1 receptor chemistry.chemical_compound Internal medicine Caffeine Glyburide Phenethylamines medicine Potassium Channel Blockers Animals Channel blocker Antihypertensive Agents Intraocular Pressure Pharmacology Pinacidil Potassium channel blocker Hypertonic saline Adenosine A2 Receptor Antagonists Endocrinology chemistry Hypotonic Solutions Alkynes Xanthines Ocular Hypertension Rabbits Hydroxy Acids Decanoic Acids Adenosine A2B receptor medicine.drug |
| Zdroj: | European journal of pharmacology. 518(2-3) |
| ISSN: | 0014-2999 |
| Popis: | 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 microl)-induced ocular hypertension (E(max): 7.7 mm Hg) 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. |
| Databáze: | OpenAIRE |
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