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This Article Full Text Full Text (PDF) All Versions of this Article: 288/4/C784    most recent 00333.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Karl, M. O. Articles by Civan, M. M. Search for Related Content PubMed PubMed Citation Articles by Karl, M. O. Articles by Civan, M. M.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Differential P1-purinergic modulation of human Schlemm's canal inner-wall cells

¹Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia; ²Department of Ophthalmology, University of Arizona, Tucson, Arizona; and ³Departments of Ophthalmology and ⁴Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Submitted 9 July 2004 ; accepted in final form 5 December 2004

Intraocular pressure is directly dependent on aqueous humor flow into, and resistance to flow out of, the eye. Adenosine has complex effects on intraocular pressure. Stimulation of A₁ and A_2A adenosine receptors changes intraocular pressure oppositely, likely through opposing actions on the outflow of aqueous humor. While the cellular sites regulating outflow resistance are unknown, the cells lining the inner wall of Schlemm's canal (SC) are a likely regulatory site. We applied selective adenosine receptor agonists to SC cells in vitro to compare the responses to A₁ and A_2A stimulation. Parallel studies were conducted with human inner-wall SC cells isolated by a novel enzyme-assisted technique and with cannula-derived mixed inner- and outer-wall SC cells. A₁ agonists increased whole cell currents of both inner-wall and cannula-derived SC cells. An A_2A agonist reduced currents most consistently in specifically inner-wall SC cells. Those currents were also increased by A_2B, but not consistently affected by A₃, stimulation. A₁, A_2A, and A₃ agonists all increased SC-cell intracellular Ca²⁺. The electrophysiological results are consistent with the possibility that inner-wall SC cells may mediate the previously reported modulatory effects of adenosine on outflow resistance. The results are also consistent with the presence of functional A_2B, as well as A₁, A_2A, and A₃ adenosine receptors in SC cells.

intraocular pressure; aqueous humor outflow; ion transport; adenosine agonists

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