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Activation of nicotinic ACh receptors with α 4 subunits induces adenosine release at the rat carotid body
Author(s) -
Conde Sílvia V,
Monteiro Emília C
Publication year - 2006
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0706676
Subject(s) - nicotinic agonist , adenosine , receptor , chemistry , carotid body , adenosine receptor , acetylcholine receptor , neuroscience , ganglion type nicotinic receptor , microbiology and biotechnology , endocrinology , pharmacology , agonist , biology , nicotinic acetylcholine receptor , biochemistry , electrophysiology
The effect of ACh on the release of adenosine was studied in rat whole carotid bodies, and the nicotinic ACh receptors involved in the stimulation of this release were characterized. ACh and nicotinic ACh receptor agonists, cytisine, DMPP and nicotine, caused a concentration‐dependent increase in adenosine production during normoxia, with nicotine being more potent and efficient in stimulating adenosine release from rat CB than cytisine and DMPP.D ‐Tubocurarine, mecamylamine, DH β E and α ‐bungarotoxin, nicotinic ACh receptor antagonists, caused a concentration‐dependent reduction in the release of adenosine evoked by hypoxia. The rank order of potency for nicotinic ACh receptor antagonists that inhibit adenosine release was DH β E>mecamylamine> D ‐tubocurarine> α ‐bungarotoxin. The effect of the endogenous agonist, ACh, which was mimicked by nicotine, was antagonized by DH β E, a selective nicotinic receptor antagonist. The ecto‐5′‐nucleotidase inhibitor AOPCP produces a 72% inhibition in the release of adenosine from CB evoked by nicotine. Taken together, these data indicate that ACh induced the production of adenosine, mainly from extracellular ATP catabolism at the CB through a mechanism that involves the activation of nicotinic receptors with α 4 and β 2 receptor subunits.British Journal of Pharmacology (2006) 147 , 783–789. doi: 10.1038/sj.bjp.0706676