ArticleBritish journal of pharmacology1994
Inhibitory effects of capsaicin on acetylcholine-evoked responses in rat phaeochromocytoma cells.
Article in British journal of pharmacology, 1994. 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, 24 citations in OpenAlex.
- Capsaicin inhibits catecholamine secretion and synthesis by blocking Na+ and Ca2+ influx through a vanilloid receptor-independent pathway in bovine adrenal medullary cells.Naunyn-Schmiedeberg's archives of pharmacology · 2006Article
- Role of vanilloid receptors in the capsaicin-mediated induction of iNOS in PC12 cells.Neurochemical research · 2004Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of capsaicin on cellular responses evoked by acetylcholine (ACh) and those by adenosine 5'-triphosphate (ATP) were investigated in rat phaeochromocytoma PC12 cells. 2. Capsaicin (1 to 30 microM) suppressed dopamine release and the intracellular Ca2+ increase evoked by 100 microM ACh. The concentration-dependence of the ACh-evoked release of dopamine was not shifted but the maximal response was reduced by capsaicin. Dopamine release evoked by 80 mM KCl was also suppressed by capsaicin (3 and 30 microM), but the extent of suppression was smaller than that of the ACh-evoked release. 3. Under whole-cell voltage-clamp, capsaicin (1 to 30 microM) reversibly inhibited the inward current activated by ACh (30 to 300 microM). The inhibition exhibited dependence on the concentration of ACh, and the current activated by a higher concentration of ACh was less inhibited. Voltage-dependence of block by capsaicin was not observed when it was tested either by applying a ramp pulse during the current activation by ACh or by eliciting the current in cells held at various potentials. 4. High concentrations of capsaicin (30 to 100 microM) enhanced the inward current as well as dopamine release evoked by 30 microM ATP. 5. The results suggest that low concentrations of capsaicin selectively antagonize responses mediated by nicotinic receptor-channels without affecting those mediated by purinoceptor-coupled channels. As the antagonism by capsaicin of the ACh-evoked responses was observed at concentrations as low as 1 microM, the influence on nicotinic receptors should be taken into account when this compound is used as a pharmacological tool to deplete neuropeptides.
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