N -Methyl-D-Aspartic Acid Receptor-Mediated Vasodilation Is Attenuated in the Retinas of Diabetic Rats.

Autor: Mori A; Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, Tokyo, Japan., Yano E; Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, Tokyo, Japan., Nishikiori M; Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, Tokyo, Japan., Fujino S; Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, Tokyo, Japan., Nakahara T; Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, Tokyo, Japan.
Jazyk: angličtina
Zdroj: Current eye research [Curr Eye Res] 2022 Aug; Vol. 47 (8), pp. 1193-1199. Date of Electronic Publication: 2022 Jun 03.
DOI: 10.1080/02713683.2022.2072896
Abstrakt: Purpose: Activation of N -methyl-d-aspartic acid (NMDA) receptors enhances nitric oxide (NO) production in retinal neuronal cells, and in turn, NO released from neuronal cells induces glial cell-mediated dilation of retinal arterioles in rats. The purpose of this study was to examine how neuronal cell-dependent, glial cell-mediated vasodilation is impacted in diabetic rat retinas.
Methods: Diabetes was induced in 6-week-old male Wistar rats by combining streptozotocin injection and D-glucose feeding. Two weeks later, the dilator function of retinal arterioles was assessed.
Results: Compared with non-diabetic rats, the dilator responses of retinal arterioles induced by intravitreal injection of NMDA and NOR3, an NO donor, were reduced in diabetic rats. Following the blockade of large-conductance Ca 2+ -activated K + (BK Ca ) channels with iberiotoxin, no significant difference in the retinal vasodilator response to NOR3 was observed between non-diabetic and diabetic rats. Intravitreal injection of 14,15-epoxyeicosatrienoic acid, a vasodilatory factor released from glial cells, dilated retinal arterioles, and the response was diminished by diabetes.
Conclusion: These findings suggest that the impaired BK Ca channel function in vascular cells is responsible for the diminished neuronal cell-dependent, glial cell-mediated dilation of retinal arterioles during the early stage of diabetes.
Databáze: MEDLINE
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