Evidence for nitroxidergic innervation in monkey ophthalmic arteries in vivo and in vitro

In anesthetized monkeys, electrical stimulation (ES) of the pterygopalatine or geniculate ganglion dilated the ipsilateral ophthalmic artery (OA). The induced vasodilatation was unaffected by phentolamine but potentiated by a tropine. Intravenous N-G-nitro-L-arginine (L-NNA) abolished the response, w hich was restored by L-arginine. Hexamethonium-abolished vasodilator respon ses induced solely by geniculate ganglionic stimulation. The L-NNA constric ted OA; L-arginine reversed the effect. Destruction of the pterygopalatine ganglion constricted the ipsilateral artery. Helical strips of OA isolated under deep anesthesia from monkeys, denuded of endothelium, responded to tr ansmural ES with relaxations, which were abolished by tetrodotoxin and L-NN A but were potentiated by atropine. It is concluded that neurogenic vasodil atation of monkey OA is mediated by nerve-derived nitric oxide (NO), and th e nerve is originated from the ipsilateral pterygopalatine ganglion that is innervated by cholinergic neurons from the brain stem via the geniculate g anglion. The OA appears to be dilated by mediation of NO continuously liber ated from nerves that receive tonic discharges from the vasomotor center. A cetylcholine liberated from postganglionic cholinergic nerves would impair the release of neurogenic NO.