GABA-Induced Relaxation of Porcine Retinal Arterioles in Vitro Depends on Inhibition from the Perivascular Retina and Is Mediated by GABACReceptors

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To study the dependence of γ-aminobutyric acid (GABA)-induced relaxation of retinal arterioles on the glutamate agonist N-methyl-D-aspartate (NMDA), adenosine triphosphate (ATP), prostaglandin E2 (PGE2), and adenosine, and to characterize the type and location of GABA-receptor(s) mediating GABA-induced relaxation of retinal arterioles. Porcine retinal arterioles were mounted in a wire myograph, and the effects of agonists and antagonists to NMDA, ATP, PGE2, and adenosine on GABA-induced relaxation were studied. Additionally, experiments were conducted to study relaxation induced by agonists to specific GABA receptors, and GABA-induced relaxation in the presence of specific GABA antagonists. Finally, immunohistochemistry was performed to identify the location of GABA(C) receptors in the porcine retina. GABA induced vasorelaxation during blocking of the glutamate NMDA receptor, PGE2 receptor, and ATP synthesis degradation, but not during blocking of the adenosine receptor or by agonists to any of these compounds. The vasorelaxing effect of GABA could be elicited by a specific GABA(C) agonist, but not by specific GABA(A) or GABA(B) agonists, and could be blocked by a specific GABA(C) antagonist, but not by specific GABA(A) or GABA(B) antagonists. GABA(C) receptor subunits could be identified in the ganglion cell layer, and at the border between the outer plexiform and inner nuclear layers. GABA-induced relaxation of porcine retinal vessels is mediated by the GABA(C) receptor in the perivascular retinal tissue, and depends on blocking of the glutamate NMDA receptor, prostaglandin E2 receptor, or ATP degradation.