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K. Holmgaard, T. Bek; L-Glutamic Acid Causes Relaxation of Porcine Retinal Arterioles Through a Nmda Receptor Dependent Mechanism. Invest. Ophthalmol. Vis. Sci. 2009;50(13):392.
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Previous studies have shown that the glutamate agonist N-metyl-D-aspartic acid, NMDA, induces a dose-dependent vasorelaxation of pre-constricted porcine retinal arterioles when surrounded by the perivascular retina. However, it is unknown whether other than NMDA glutamate receptors are involved in this vasorelaxation.
Porcine retinal arterioles with preserved perivascular retinal tissue were mounted in a wire myograph for isometric force measurements. After constriction of the arterioles with U46619, a thromboxane analogue, the vasodilating effects of L-glutamic acid combined with antagonists to respectively the NMDA-, metabotropic, and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-/kinate glutamat receptors were studied. In each experiment the perivascular retinal tissue was removed, and the experiment was repeated on the isolated arteriole.
L-glutamic acid induced a dose-dependent vasorelaxation, p<0.001 repeated measures ANOVA, (EC50=118.62 µM), which disappeared when the perivascular retina was removed. The NMDA receptor blocker, DL-APV, caused a significant reduction of L-glutamic acid induced vasorelaxation (p=0.033 and 0.048 at 10-3 and 3 x 10-3 M concentrations, respectively), whereas no effect on the glutamate induced vasorelaxation was induced by neither the metabotropic antagonist MCPG (p≥0.1) nor the AMPA / kinate receptor antagonist CNQX (p≥0.11).
The findings suggest that the vasorelaxing effect of L-glutamic acid on pre-constricted porcine retinal arterioles in vitro depends on the perivascular retinal tissue and is mediated through a direct action on the glutamate NMDA receptor, but not metabotropic or AMPA/kinate receptors.The findings contributes to the understanding of the tone regulation of retinal arterioles and may potentially help identifying mechanisms for controlling perfusion disturbances in retinal vascular disease.
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