Neural nitric oxide mediates Edinger-Westphal nucleus evoked increase in choroidal blood flow in the pigeon

Yuri S. Zagvazdin, Malinda E C Fitzgerald, Giuseppe Sancesario, Anton Reiner

Research output: Contribution to journalArticle

62 Citations (Scopus)

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 an 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, N(g)-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 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.

Original languageEnglish (US)
Pages (from-to)666-672
Number of pages7
JournalInvestigative Ophthalmology and Visual Science
Volume37
Issue number4
StatePublished - Mar 1996

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Columbidae
Nitric Oxide
NG-Nitroarginine Methyl Ester
Nitric Oxide Synthase
Arginine
Parasympathetic Nervous System
Laser-Doppler Flowmetry
Edinger-Westphal Nucleus
Nerve Fibers
Vasodilation
Electric Stimulation
Neurotransmitter Agents
Up-Regulation
Blood Pressure

All Science Journal Classification (ASJC) codes

  • Ophthalmology

Cite this

Neural nitric oxide mediates Edinger-Westphal nucleus evoked increase in choroidal blood flow in the pigeon. / Zagvazdin, Yuri S.; Fitzgerald, Malinda E C; Sancesario, Giuseppe; Reiner, Anton.

In: Investigative Ophthalmology and Visual Science, Vol. 37, No. 4, 03.1996, p. 666-672.

Research output: Contribution to journalArticle

Zagvazdin, Yuri S. ; Fitzgerald, Malinda E C ; Sancesario, Giuseppe ; Reiner, Anton. / Neural nitric oxide mediates Edinger-Westphal nucleus evoked increase in choroidal blood flow in the pigeon. In: Investigative Ophthalmology and Visual Science. 1996 ; Vol. 37, No. 4. pp. 666-672.
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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 an 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, N(g)-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 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.",
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AU - Reiner, Anton

PY - 1996/3

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N2 - 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 an 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, N(g)-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 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.

AB - 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 an 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, N(g)-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 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.

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