ArticleBritish journal of pharmacology1999
Multiple calcium channels regulate neurotransmitter release from vagus nerve terminals in the cat bronchiole.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 14 citations in OpenAlex.
- Effect of rocuronium on the level and mode of pre-synaptic acetylcholine release by facial and somatic nerves, and changes following facial nerve injury in rabbits.International journal of clinical and experimental pathology · 2015Article
- Calcium channel subtypes for cholinergic and nonadrenergic noncholinergic neurotransmission in isolated guinea pig trachea.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
1. Twitch-like contractions and non-adrenergic non-cholinergic (NANC) relaxations evoked by electrical field stimulation (EFS) of the cat bronchiole were used to examine the voltage-activated calcium channels involved in excitatory and inhibitory neurotransmission in the cat bronchiole. 2. Nifedipine (50 microM), the L-type calcium channel antagonist, did not affect the twitch-like contraction and NANC relaxations. However, low concentrations of the N-type calcium channel blocker omega-conotoxin GVIA (omega-CgTX GVIA) (0.1 microM) irreversibly abolished twitch-like contractions evoked by trains of EFS </=10 stimuli at 20 Hz. 3. After the prolonged treatment with 0.1 microM omega-CgTX GVIA, EFS evoked initial fast and later slow NANC relaxations in the presence of 5-HT (10 microM), atropine and guanethidine (1 microM each). However increased concentration of omega-CgTX GVIA (1 microM) completely suppressed the slow NANC relaxation without affecting the initial fast component. 4. omega-agatoxin IVA (100 nM), the P- and Q-type calcium channel inhibitor, and nimodipine (10 microM), the L- and T-type calcium channel blocker, did not affect the amplitude of the initial fast NANC relaxation in the absence or presence of omega-CgTX GVIA (1 microM). 5. The contraction or relaxation induced by exogenous acetylcholine (ACh) (0.5 microM) or the nitric oxide donor, s-nitroso-N-acetyl penicillamine (SNAP) (1 microM) were not affected by omega-CgTX GVIA (1 microM). 6. Taken together, these results suggest that generation of twitch-like contraction and later slow NANC relaxation are regulated by N-type calcium channels, whereas generation of the initial fast NANC relaxation possibly involves R-type calcium channel.
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