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- Title
Role of voltage-dependent calcium channels in stimulus–secretion coupling in rabbit carotid body chemoreceptor cells.
- Authors
Rocher, Asunción; Geijo-Barrientos, Emilio; Cáceres, Ana; Rigual, Ricardo; González, Constancio; Almaraz, Laura
- Abstract
We 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 200μmCd2+. L-type channels (sensitive to 2μmnisoldipine) activated at–30 mV and carried 21± 2% of totalICa. Non-L-type channels activated at potentials positive to–10 mV and carried: N channels (sensitive to 1μmω-conotoxin-GVIA) 16± 1% of totalICa, P/Q channels (sensitive to 3μmω-conotoxin-MVIIC after nisoldipine plus GVIA) 23± 3% of totalICa and R channels (resistant to all blockers combined) 40± 3% of totalICa. CA release induced by hypoxia, hypercapnic acidosis, dinitrophenol (DNP) and high K+o in the intact CB was inhibited by 79–98% by 200μmCd2+. 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 mmK+o brought resting membrane potential (Em) of chemoreceptor cells (–48.1± 1.2 mV) to–22.5 and+7.2 mV, respectively. Thirty millimolar K+o-evoked release was abolished by nisoldipine but that induced by 100 mmK+o 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.
- Subjects
CALCIUM channels; ION channels; ACTIVE biological transport; CAROTID body; CHEMORECEPTORS; RABBITS
- Publication
Journal of Physiology, 2005, Vol 562, Issue 2, p407
- ISSN
0022-3751
- Publication type
Article
- DOI
10.1113/jphysiol.2004.075523