ArticleThe Journal of physiology1999
Acid-evoked quantal catecholamine secretion from rat phaeochromocytoma cells and its interaction with hypoxia-evoked secretion.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed, 28 citations in OpenAlex.
- Simulations of amperometric monitoring of exocytosis: moderate pH variations within the cell-electrode cleft with the buffer diffusion.Analytical and bioanalytical chemistry · 2021Article
- Downregulation of the Central Noradrenergic System byInfection and immunity · 2019Article
- Article
- Reproducing increased dopamine with infection to evaluate the role of parasite-encoded tyrosine hydroxylase activity.Infection and immunity · 2015Article
- Rat adrenal chromaffin cells are neonatal CO2 sensors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Amperometric recordings using polarized carbon fibre microelectrodes were used to detect exocytosis of catecholamines from rat phaeochromocytoma (PC12) cells in response to a reduction in pHo. 2. Exocytosis was detected at pHo levels of between 7.2 and 6.8. This was probably due to intracellular acidification, since acid-evoked secretion was enhanced by the Na+-H+ exchange blocker ethylisopropylamiloride (30 microM), and was mimicked by sodium propionate (10 mM), which causes selective intracellular acidosis. 3. Acid-evoked exocytosis was abolished by removal of Ca2+o or application of 200 microM Cd2+. It was unaffected by nifedipine, but significantly reduced by either omega-conotoxin GVIA (1 microM) or omega-agatoxin GIVA (200 nM). The two toxins applied together almost completely abolished (> 97 %) acid-evoked secretion. 4. Hypoxia-evoked catecholamine release was potentiated under acidic conditions and suppressed under alkaline conditions in a manner which indicated a greater than additive interaction of these two stimuli. 5. Our results indicate that, like carotid body arterial chemoreceptors, PC12 cells represent model chemoreceptor cells for both hypoxia and acidity and that the release of catecholamines in response to these physiological stimuli is dependent on Ca2+ influx through voltage-gated N- and P/Q-type Ca2+ channels.
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