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Abstract
PURPOSE: Nitric oxide (NO) has been identified as a putative neurotransmitter in choroidal perivascular nerve fibers originating parasympathetically. Although constitutively produced NO has been implicated in the regulation of the choroidal circulation, the specific role of neurally derived NO in choroidal vasodilation has not been determined. This study examined the role of neurally derived NO in the control of the choroidal blood flow (ChBF) in vivo. METHODS: Resting ChBF and a increase in ChBF elicited by electrical stimulation of the nucleus of Edinger-Westphal (EW) were measured transclerally by laser Doppler flowmetry in anesthetized pigeons before and after administration of a selective inhibitor of neural NO synthase, 7-Nitroindazole (7NI; 50 mg/kg given intraperitoneally); a nonselective NO synthase inhibitor, Ng-nitro-L-arginine methyl ester (L-NAME; 30 mg/kg given intravenously); L-arginine (300 mg/kg given intravenously) followed by 7NI (50 mg/kg given intraperitoneally); or vehicle. RESULTS: The 7NI and L-NAME, but not the vehicle, attenuated the EW-evoked response (maximally by 78% and 83%, respectively), and this effect lasted for at least 1 hour. Pretreatment with L-arginine abolished this effect of 7NI. Resting ChBF was reduced and systemic blood pressure was increased after L-NAME administration, but both were unchanged after 7NI or vehicle were administered. CONCLUSIONS: Neurally derived NO is responsible for a major component of the ChBF increase caused by EW stimulation in pigeons. This represents the first demonstration in vivo that neuronally produced NO is an important factor in the control of ChBF by the parasympathetic nervous system. In particular, neuronally produced NO appears to play a role in rapid upregulation of ChBF in the pigeon, whereas endothelially produced NO plays a major role in control of resting ChBF.