A1 adenosine receptors (ARs) reduce, and A2ARs increase intraocular pressure, partly by differentially altering resistance to aqueous humor outflow. It is unknown whether the opposing effects of A1AR and A2AR agonists are mediated at different outflow-pathway cell targets or by opposing actions on a single cell target. We tested whether a major outflow-pathway cell, the trabecular meshwork (TM) cell might constitute the primary AR-agonist target and respond differentially to A1, A2Aa and A3AR agonists. Receptor activation in human TM cells was identified by applying subtype-selective AR agonists: CPA and ADAC for A1 ARs, CGS 21680 and DPMA for A2AARs, and Cl-IB-MECA and IB-MECA for A3ARs. Stimulation of A1 A2A and A3ARs elevated Ca2+, measured with fura-2. Whole-cell patch clamping indicated that AR agonists activated ion channels non-uniformly, possibly reflecting variability in magnitude of agonist-triggered second-messenger responses. A], A2A and A3AR agonists all reduced volume, determined by calcein cell imaging. The endogenous source of adenosine delivery to the outflow pathway could be the TM cells since these cells were stimulated to release ATP by hypotonic perfusion. We conclude that: (1) TM cells express functional A1, A2A and A3ARs; and (2) the reported differential effects of AR agonists on aqueous humor outflow are not mediated by differential actions on TM-cell Ca2+ and volume, but likely by actions on separate cell targets.
The Journal of Membrane Biology – Springer Journals
Published: Mar 25, 2002
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