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Muscarinic and nicotinic receptors raise intracellular Ca2+ levels in rat carotid body type I cells.
Author(s) -
Dasso L L,
Buckler K J,
Vaughan-Jones R D
Publication year - 1997
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.1997.sp021861
Subject(s) - muscarinic acetylcholine receptor , acetylcholine , nicotinic agonist , muscarinic agonist , muscarine , mecamylamine , nicotinic antagonist , endocrinology , chemistry , medicine , cholinergic , muscarinic acetylcholine receptor m3 , muscarinic antagonist , intracellular , stimulation , muscarinic acetylcholine receptor m1 , muscarinic acetylcholine receptor m2 , agonist , alpha 4 beta 2 nicotinic receptor , receptor , biology , nicotinic acetylcholine receptor , biochemistry
1. The effects of cholinergic agonists upon intracellular free Ca2+ levels ([Ca2+]i) have been studied in enzymically isolated rat carotid body single type I cells, using indo‐1. 2. Acetylcholine (ACh) dose‐dependently increased [Ca2+]i in 55% of cells studied (EC50 = 13 microM). These [Ca2+]i rises were partially inhibited by atropine or mecamylamine. 3. Specific nicotinic and muscarinic agonists also elevated [Ca2+]i in a dose‐dependent manner (nicotine, EC50 = 15 microM; methacholine, EC50 = 20 microM). 4. While the majority of the ACh‐sensitive cells responded to both classes of cholinergic agonist, 29% responded exclusively to nicotinic stimulation and 9% responded exclusively to muscarinic stimulation. 5. In the presence of nicotinic agonists, Ca2+i responses were transient. In the presence of muscarinic agonists, Ca2+i responses consisted of an initial rise, which then declined to a lower plateau level. 6. Nicotinic responses were rapidly abolished in Ca(2+)‐free medium, suggesting that they are dependent on Ca2+ influx. 7. The plateau component of the muscarinic‐activated response was also abolished in Ca(2+)‐free conditions. The rapid initial [Ca2+]i rise, however, could still be evoked after several minutes in Ca(2+)‐free medium. Muscarine also increased Mn2+ quenching of intracellular fura‐2 fluorescence. These data suggest that the full muscarinic response depends on both Ca2+ release from intracellular stores and Ca2+o influx. 8. The results indicate that, in rat carotid body type I cells, both nicotinic and muscarinic acetylcholine receptors increase [Ca2+]i, but achieve this via different mechanisms. ACh may therefore play a role in carotid body function by modulating Ca2+i in the chemosensory type I cells.