ラット網膜におけるグリア細胞を介する血管拡張にはプロスタノイド EP₂ 受容体刺激が関与する

抄録

We have previously found that nitric oxide (NO) derived from neuronal cells acts on glial cells and causes vasodilation in the rat retina via release of epoxyeicosatrienoic acids (EETs) and prostaglandins. The aim of this study was to identify the prostanoid receptors involved in the NO-induced glial cell-derived vasodilation in the rat retina.

We used male Wistar rats to examine the effects of intravitreal pretreatment of indomethacin, a cyclooxygenase inhibitor, PF-04418948, a prostanoid EP₂ receptor antagonist, and CAY10441, a prostanoid IP receptor antagonist, on the changes in the retinal arteriolar diameter induced by intravitreal injection of NOR3, an NO doner. The retinal arteriolar diameters were measured using the ocular fundus images captured with a high-resolution digital camera in vivo.

Increase in the retinal arteriolar diameter induced by intravitreal injection of NOR3 was significantly suppressed by intravitreal pretreatment of indomethacin and PF-04418948, but not CAY10441.

These results suggested that activation of arachidonic acid cascade and subsequent stimulation of prostanoid EP₂ receptors are involved in the rat retinal vasodilatory responses evoked by NO-induced glial cells stimulation. Thus, glial cells-derived prostaglandin E₂ may play important roles in the retinal vasodilatory mechanisms.