Abstract
Current concepts on the location and functional significance of nicotinic receptors in the carotid body rest on α-bungarotoxin binding and autoradiographic studies. Using an in vitro preparation of the cat carotid body whose catecholamine deposits have been labeled by prior incubation with the tritiated natural precursor [ 3H]tyrosine, we have found that nicotine induces release of [ 3H]catecholamines in a dose-dependent manner (IC 50=9.81 μM). We also found that mecamylamine (50 μM) completely abolished the nicotine-induced release, while α-bungarotoxin (100 nM; ≈20 times its binding K d) only reduced the release by 56%. These findings indicate that chemoreceptor cells, and perhaps other carotid body structures, contain nicotinic receptors that are not sensitive to α-bungarotoxin and force a revision of the current concepts on cholinergic mechanisms in the carotid body chemoreception.
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