Mechanism of nitric oxide-induced dilation of rat retinal blood vessels in vivo

Nitric Oxide (NO) has been reported to stimulate synthesis of prostacyclin (PGI2) in ocular blood vessels in vitro, however, physiological significance of this phenomenon has not yet been elucidated. In the present study, we examined whether NO stimulates PGI2 synthesis in rat retinal blood vessels by means of a novel images of small animals. Male Wistar rats (8-10 weeks old) were anesthetized with thiobutabarbital (120 mg/kg, i. p. ). Fundus images were captured by Nikon D1 digital camera that was equipped with a special objective lens. Diameters of retinal arterioles and venules were estimated on a Macintosh computer with image processing softwares. Intravenous infusions of sodium nitropmsside (1-100μg /kg/min), an NO donor, increased diameters of both retinal arterioles and venules and lowered mean arterial pressure (MAP) in a dose-dependent manner. Indomethacin (5 mg/kg, i. v. ), a cyclooxygenase inhibitor, attenuated dilation of retinal blood vessels, but failed to affect hypotensive effect of SNP. The diminished responses to SNP of retinal blood vessels observed after indomethacin treatment was not restored under intravenous infusions of PGI2 (0. 1 and 0. 3μg/kg/min). These data suggest that, in contrast to peripheral blood vessles, NO relaxes retinal arterioles and venules mainly through augmented production of vasodilating prostaglandins, probably PGI2, that results from activation of cyclooxygenase.