Adrenergic and nitrergic neurotransmitters are released by the autonomic system of the pig long posterior ciliary artery

Er-Ning Su, V.A. Alder, Dao-Yi Yu, Stephen Cringle

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

The role played by adrenergic, muscarinic and nitric oxide putative neurotransmitters released from autonomic nerve endings onto the pig proximal long posterior ciliary artery (LPCA) was determined. The proximal LPCA in the pig usually supplies both the uveal and retinal circulations. In this study, in vitro ring segments of the artery, passively stretched and with noradrenaline-induced tone, were neurogenically stimulated (NS) using electrical field stimulation with 5-sec trains of 0.2 msec pulses. NS produced a frequency dependent contraction in all vessels which was completely abolished by 10(-6) M tetrodotoxin. 40 Hz stimulation was used throughout the study as it produced a maximal NS contraction. 10(-5) M guanethidine abolished the NS-induced contraction and revealed a NS-induced relaxation, as did the or adrenergic blocker, phentolamine, in vessels passively stretched. The beta adrenergic blocker, propranolol, only slightly reduced the NS-induced constriction. In vessels pre-contracted with noradrenaline, NS produced a relaxation (D) which was proportional in magnitude to the tone (C) viz. D = (0.30 +/- 0.04) . C + (0.24 +/- 0.06). The muscarinic blocker, atropine, had no effect on the NS-induced relaxation, implying that it is a non-adrenergic, non-cholinergic mediated system. Incubation with N-w-nitro-L-arginine methyl ester reduced the NS-induced relaxation to 48% of its control value, a reduction which was reversed in the presence of excess L-arginine. Damage to endothelial cell function did not reduce the NS-induced relaxation. It is concluded that the autonomic innervation of the proximal LPCA releases both contraction and relaxation neurotransmitters. Contraction is mediated by an ai adrenergic neurotransmitter. At least two neurotransmitters mediate relaxation, one of which is probably nitric oxide. There is no functional evidence for the release of beta adrenergic neurotransmitter from the sympathetic system or acetylcholine from the parasympathetic system.
Original languageEnglish
Pages (from-to)907-917
JournalCurrent Eye Research
Volume13
Issue numberNot known
DOIs
Publication statusPublished - 1994

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Ciliary Arteries
Adrenergic Agents
Neurotransmitter Agents
Swine
Cholinergic Agents
Norepinephrine
Nitric Oxide
Guanethidine
Autonomic Pathways
Adrenergic beta-Antagonists
Adrenergic Antagonists
Nerve Endings
Phentolamine
Tetrodotoxin
Atropine
Constriction
Propranolol
Electric Stimulation
Acetylcholine
Arginine

Cite this

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title = "Adrenergic and nitrergic neurotransmitters are released by the autonomic system of the pig long posterior ciliary artery",
abstract = "The role played by adrenergic, muscarinic and nitric oxide putative neurotransmitters released from autonomic nerve endings onto the pig proximal long posterior ciliary artery (LPCA) was determined. The proximal LPCA in the pig usually supplies both the uveal and retinal circulations. In this study, in vitro ring segments of the artery, passively stretched and with noradrenaline-induced tone, were neurogenically stimulated (NS) using electrical field stimulation with 5-sec trains of 0.2 msec pulses. NS produced a frequency dependent contraction in all vessels which was completely abolished by 10(-6) M tetrodotoxin. 40 Hz stimulation was used throughout the study as it produced a maximal NS contraction. 10(-5) M guanethidine abolished the NS-induced contraction and revealed a NS-induced relaxation, as did the or adrenergic blocker, phentolamine, in vessels passively stretched. The beta adrenergic blocker, propranolol, only slightly reduced the NS-induced constriction. In vessels pre-contracted with noradrenaline, NS produced a relaxation (D) which was proportional in magnitude to the tone (C) viz. D = (0.30 +/- 0.04) . C + (0.24 +/- 0.06). The muscarinic blocker, atropine, had no effect on the NS-induced relaxation, implying that it is a non-adrenergic, non-cholinergic mediated system. Incubation with N-w-nitro-L-arginine methyl ester reduced the NS-induced relaxation to 48{\%} of its control value, a reduction which was reversed in the presence of excess L-arginine. Damage to endothelial cell function did not reduce the NS-induced relaxation. It is concluded that the autonomic innervation of the proximal LPCA releases both contraction and relaxation neurotransmitters. Contraction is mediated by an ai adrenergic neurotransmitter. At least two neurotransmitters mediate relaxation, one of which is probably nitric oxide. There is no functional evidence for the release of beta adrenergic neurotransmitter from the sympathetic system or acetylcholine from the parasympathetic system.",
author = "Er-Ning Su and V.A. Alder and Dao-Yi Yu and Stephen Cringle",
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Adrenergic and nitrergic neurotransmitters are released by the autonomic system of the pig long posterior ciliary artery. / Su, Er-Ning; Alder, V.A.; Yu, Dao-Yi; Cringle, Stephen.

In: Current Eye Research, Vol. 13, No. Not known, 1994, p. 907-917.

Research output: Contribution to journalArticle

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AB - The role played by adrenergic, muscarinic and nitric oxide putative neurotransmitters released from autonomic nerve endings onto the pig proximal long posterior ciliary artery (LPCA) was determined. The proximal LPCA in the pig usually supplies both the uveal and retinal circulations. In this study, in vitro ring segments of the artery, passively stretched and with noradrenaline-induced tone, were neurogenically stimulated (NS) using electrical field stimulation with 5-sec trains of 0.2 msec pulses. NS produced a frequency dependent contraction in all vessels which was completely abolished by 10(-6) M tetrodotoxin. 40 Hz stimulation was used throughout the study as it produced a maximal NS contraction. 10(-5) M guanethidine abolished the NS-induced contraction and revealed a NS-induced relaxation, as did the or adrenergic blocker, phentolamine, in vessels passively stretched. The beta adrenergic blocker, propranolol, only slightly reduced the NS-induced constriction. In vessels pre-contracted with noradrenaline, NS produced a relaxation (D) which was proportional in magnitude to the tone (C) viz. D = (0.30 +/- 0.04) . C + (0.24 +/- 0.06). The muscarinic blocker, atropine, had no effect on the NS-induced relaxation, implying that it is a non-adrenergic, non-cholinergic mediated system. Incubation with N-w-nitro-L-arginine methyl ester reduced the NS-induced relaxation to 48% of its control value, a reduction which was reversed in the presence of excess L-arginine. Damage to endothelial cell function did not reduce the NS-induced relaxation. It is concluded that the autonomic innervation of the proximal LPCA releases both contraction and relaxation neurotransmitters. Contraction is mediated by an ai adrenergic neurotransmitter. At least two neurotransmitters mediate relaxation, one of which is probably nitric oxide. There is no functional evidence for the release of beta adrenergic neurotransmitter from the sympathetic system or acetylcholine from the parasympathetic system.

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