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Acid‐evoked quantal catecholamine secretion from rat phaeochromocytoma cells and its interaction with hypoxia‐evoked secretion
Author(s) -
Taylor S. C.,
Roberts M. L.,
Peers C.
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.0765n.x
Subject(s) - exocytosis , chemoreceptor , secretion , catecholamine , carotid body , endocrinology , medicine , nifedipine , chemistry , hypoxia (environmental) , intracellular , sodium propionate , intracellular ph , electrophysiology , propionate , biology , calcium , biochemistry , receptor , organic chemistry , oxygen
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 pH o . 2 Exocytosis was detected at pH o 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 μ m ), and was mimicked by sodium propionate (10 mM), which causes selective intracellular acidosis. 3 Acid‐evoked exocytosis was abolished by removal of Ca 2+ o or application of 200 μ m Cd 2+ . It was unaffected by nifedipine, but significantly reduced by either ω‐conotoxin GVIA (1 μ m ) or ω‐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 Ca 2+ influx through voltage‐gated N‐ and P/Q‐type Ca 2+ channels.