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Title

Role of voltage-dependent calcium channels in stimulus-secretion coupling in rabbit carotid body chemoreceptor cells

AuthorsRocher, Asunción CSIC ORCID; Geijo-Barrientos, Emilio; Cáceres, Ana Isabel; Rigual, Ricardo CSIC ORCID; González, Constancio CSIC; Almaraz, Laura
Issue Date2005
PublisherWiley-Blackwell
CitationJournal of Physiology 562(2): 407-420 (2005)
AbstractWe have defined Ca2+ channel subtypes expressed in rabbit carotid body (CB) chemoreceptor cells and their participation in the stimulus-evoked catecholamine (CA) release. Ca2+ currents (ICa) activated at -30 mV, peaked at +10 mV and were fully blocked by 200 μM Cd2+. L-type channels (sensitive to 2 μM nisoldipine) activated at -30 mV and carried 21 ± 2% of total ICa. Non-L-type channels activated at potentials positive to -10 mV and carried: N channels (sensitive to 1 μM ω-conotoxin-GVIA) 16 ± 1% of total ICa, P/Q channels (sensitive to 3 μM ω-conotoxin-MVIIC after nisoldipine plus GVIA) 23 ± 3% of total ICa and R channels (resistant to all blockers combined) 40 ± 3% of total ICa. CA release induced by hypoxia, hypercapnic acidosis, dinitrophenol (DNP) and high Ko + in the intact CB was inhibited by 79-98% by 200 μM Cd2+. Hypoxia, hypercapnic acidosis and DNP, depolarized chemoreceptor cells and eventually generated repetitive action potential discharge. Nisoldipine plus MVIIC nearly abolished the release of CAs induced by hypoxia and hypercapnic acidosis and reduced by 74% that induced by DNP. All these secretory responses were insensitive to GVIA. 30 and 100 mM Ko + brought resting membrane potential (Em) of chemoreceptor cells (-48.1 ± 1.2 mV) to -22.5 and +7.2 mV, respectively. Thirty millimolar Ko +-evoked release was abolished by nisoldipine but that induced by 100 mM Ko + was mediated by activation of L, N, and P/Q channels. Data show that tested stimuli depolarize rabbit CB chemoreceptor cells and elicit CA release through Ca2+ entry via voltage-activated channels. Only L and P/Q channels are tightly coupled to the secretion of CA. © The Physiological Society 2004.
URIhttp://hdl.handle.net/10261/72754
DOIhttp://dx.doi.org/10.1113/jphysiol.2004.075523
Identifiersdoi: 10.1113/jphysiol.2004.075523
issn: 0022-3751
e-issn: 1469-7793
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