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L‐ and N‐type Ca2+ channels in adult rat carotid body chemoreceptor type I cells.
Author(s) -
e Silva M J,
Lewis D L
Publication year - 1995
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 - 10.1113/jphysiol.1995.sp021083
Subject(s) - dihydropyridine , nimodipine , chemistry , membrane potential , biophysics , chemoreceptor , voltage dependent calcium channel , electrophysiology , carotid body , patch clamp , agonist , endocrinology , calcium , medicine , biology , biochemistry , receptor , organic chemistry
1. Whole‐cell voltage‐dependent Ca2+ currents recorded from chemoreceptor type I cells of the adult rat carotid body had maximum amplitudes of ‐94 pA in 10 mM Ca2+ and were half‐inactivated at a holding potential of ‐38 mV. Somatostatin and dopamine inhibited whole‐cell Ca2+ current in type I cells. 2. The dihydropyridine agonist (+)202‐791 increased the Ca2+ current amplitude by 106% at a step potential of ‐18 mV. The dihydropyridine antagonist nimodipine decreased the Ca2+ current amplitude by 40% from a holding potential of ‐80 mV, and by 74% from a holding potential of ‐60 mV. The nimodipine‐sensitive current had a maximum amplitude at a membrane potential of ‐12 mV. omega‐Conotoxin GVIA (omega‐CgTX GVIA) blocked the whole‐cell Ca2+ current by 40%. The omega‐CgTX GVIA‐sensitive current had a maximum amplitude at a membrane potential of +2 mV. 3. In summary, type I cells of the adult rat carotid body have dihydropyridine‐sensitive L‐type and omega‐conotoxin GVIA‐sensitive N‐type voltage‐dependent Ca2+ channels. These channels may play a role in the voltage‐gated entry of Ca2+ necessary for stimulus‐secretion coupling in response to changes in arterial PO2, PCO2 and pH. Inhibition of the Ca2+ currents by somatostatin and dopamine may alter the chemotransduction signal in type I cells.