Autoregulation of Cholinergic Neurotransmission in Airways Nerves

Watson, N.

doi:10.1007/978-3-0348-7558-5_10

Cited by 2 publications

(1 citation statement)

References 71 publications

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“…Acetylcholine release upon stimulation of parasympathetic nerves within the airways is subject to modulation by the activation of prejunctional autoinhibitory muscarinic M2 receptors (Watson, 1994). Because of this, studies directed towards examining the effects of various factors enhancing the release of acetylcholine from pulmonary cholinergic neurones are complicated by autoinhibition of transmitter release.…”

Section: Discussionmentioning

confidence: 99%

Influence of respiratory tract viral infection on endothelin‐1‐induced potentiation of cholinergic nerve‐mediated contraction in mouse trachea

Carr¹,

Goldie²,

Henry³

1996

British J Pharmacology

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1 This study examined the influence of respiratory tract infection with influenza A/PR-8/34 virus on endothelin receptor-mediated modulation of contraction induced by stimulation of cholinergic nerves in mouse isolated trachea. 2 The ETB receptor-selective agonist, sarafotoxin S6c (30 nM) induced large transient contractions (118 + 5% Cma_, n = 13; where C.,, is the contraction induced by 10 gM carbachol) of isolated tracheal segments from control mice. The peak contractile response to 30 nM sarafotoxin S6c was significantly lower in preparations from virus-inoculated mice at day 2 (57+8% Cm,,x, n = 3, P< 0.05) and 4 postinoculation (90 + 8% Cm,a,, n = 9, P< 0.05), consistent with virus-induced attentuation of the ETB receptor-effector system linked to airway smooth muscle contraction. The mean peak contraction to 30 nM sarafotoxin S6c of preparations from virus-inoculated mice at day 8 post-inoculation (94+17% Cm,,,a, n=4) was not significantly different from that of control.3 Electrical field stimulation (EFS; 90 V, 0.5 ms duration, 10 s train, 0.1 -30 Hz) of preparations from control and virus-inoculated mice, caused contractions that were abolished by 0.1 HIM atropine or 3 gM tetrodotoxin, indicating that these responses were mediated by neuronally released acetylcholine. Sarafotoxin S6c markedly potentiated contractions induced by a standard stimulus (0.3 Hz, every 3 min) in tracheal segments from control and virus-inoculated mice. In tracheal tissue from control mice, 30 nM sarafotoxin S6c significantly increased a standard EFS-induced contraction of 24+4% Cmax by a further 24+3% C,,, (i.e. 2 fold increase, n = 11). Sarafotoxin S6c (30 nM) also markedly potentiated standard EFS-induced contractions in preparations from virus-inoculated mice at day 2 (17 + 2% Cma, n = 3), day 4 (17 + 5% Cmax, n = 9) and day 8 (26 + 5% Cm.,,, n = 4) post-inoculation. The level of potentiation of EFS-induced contractions in preparations from virus-inoculated mice was similar to that in tissue from control mice at days, 2, 4 and 8 post-inoculation. In contrast, sarafotoxin S6c (30 nM) did not enhance contractile responses of tracheal segments from control and virus-inoculated mice to exogenously applied acetylcholine (n = 3). 4 Endothelin-1 (1 nM) caused similar potentiations of standard EFS-induced contractions in tracheal segments from control (13 + 2% Cma,,, n = 23) and virus-inoculated mice at day 2 (13+1% Cm, n=5), day 4 (16+5% Cmax, n=6), and day 8 (13+3% Cma,, n=8) post-inoculation. In contrast, 1 nM endothelin-I did not enhance contractile responses of tracheal segments from control and virusinoculated mice to exogenously applied acetylcholine (n = 4). Neither the ETA receptor-selective antagonist, BQ-123 (3 gM) nor the ETB receptor-selective antagonist, BQ-788 (1 gM) alone had any significant inhibitory effect on endothelin-l-induced potentiations of tracheal segments from control or virus-inoculated mice at days 2, 4 and 8 post-inoculation. However, simultaneous pre-incubation with BQ-123 (3 pM) and BQ-788 (1 gIM) p...

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Section: Discussionmentioning

confidence: 99%

Influence of respiratory tract viral infection on endothelin‐1‐induced potentiation of cholinergic nerve‐mediated contraction in mouse trachea

Carr¹,

Goldie²,

Henry³

1996

British J Pharmacology

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Influence of the epithelium on acetylcholine release from parasympathetic nerves of the rat trachea

Vlahos

Fabiani

Story

2000

Journal of Autonomic Pharmacology

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1. The present study was undertaken to investigate the influence of the airway epithelium on the release of acetylcholine (ACh) from parasympathetic nerves of the rat trachea. Epithelium-intact and epithelium-denuded preparations of rat trachea were incubated with [3H]-choline to incorporate [3H]-ACh into the cholinergic transmitter stores. Release of radiolabelled transmitter ACh was evoked by electrical field stimulation (60 s trains of 1 ms pulses, 5 Hz, 15 V). 2. Field stimulation both of epithelium-intact and epithelium-denuded radiolabelled tracheal preparations evoked an increase in the efflux of radioactivity; however, the mean stimulation-induced (S-I) efflux from epithelium-denuded preparations (2932 +/- 190 d.p.m., n = 9) was approximately 60% of that from epithelium-intact preparations (4802 +/- 820 d.p.m., n = 11). We have shown previously that, in epithelium-intact (but not epithelium-denuded) tracheal preparations, a substantial proportion of the S-I efflux is resistant to tetrodotoxin (1 microM) and to the removal of extracellular Ca2+, indicating that much of the S-I efflux is not caused by exocytotic release of neuronal [3H]-ACh. In epithelium-denuded tracheal preparations, superfused individually, phosphorylcholine (1 and 100 microM) did not alter S-I efflux. In epithelium-intact tracheal preparations, both in the absence and in the presence of atropine (1 microM), neither N(G)-nitro-L-arginine (100 microM), superoxide dismutase (100 units ml(-1)), indomethacin (10 microM), capsaicin (30 microM) nor alpha-chymotrypsin (1 unit ml(-1)) altered S-I efflux. 3. Experiments were also performed using two tracheal preparations superfused in series. When unlabelled epithelium-intact preparations were present in the upper chamber (superfused first), the S-I efflux from radiolabelled epithelium-denuded preparations in the lower chamber (superfused second) did not differ significantly from radiolabelled epithelium-denuded preparations superfused individually. Moreover, there was no significant difference in the S-I efflux from radiolabelled epithelium-denuded preparations in the lower chamber between experiments in which the upper chamber contained epithelium-intact or epithelium-denuded preparations. 4. Field stimulation of epithelium-intact tracheal preparations in the upper chamber with 90, 120 and 300-s periods (trains of 1 ms pulses, 5 Hz, 15 V) did not significantly alter the S-I efflux from radiolabelled epithelium-denuded tracheal preparations in the lower chamber. 5. When introduced into the upper (unlabelled epithelium-intact) and subsequently allowed to superfuse the lower (radiolabelled epithelium-denuded) tracheal preparations, the stable cholinomimetic carbachol (3 microM) markedly reduced the S-I efflux whereas ACh (0.1 and 1 microM) had no significant effect. However, in the presence of the anti-cholinesterase neostigmine (1 microM), ACh (1 microM) significantly reduced S-I efflux, indicating that ACh is subject to rapid hydrolysis by cholinesterase enzymes. When atropine (10 microM) was on...

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Autoregulation of Cholinergic Neurotransmission in Airways Nerves

Cited by 2 publications

References 71 publications

Influence of respiratory tract viral infection on endothelin‐1‐induced potentiation of cholinergic nerve‐mediated contraction in mouse trachea

Influence of respiratory tract viral infection on endothelin‐1‐induced potentiation of cholinergic nerve‐mediated contraction in mouse trachea

Influence of the epithelium on acetylcholine release from parasympathetic nerves of the rat trachea

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