Localization and function of cat carotid body nicotinic receptors.
Acetylcholine and nicotinic agents excite cat carotid body chemoreceptors and modify their response to natural stimuli. The present experiments utilized [125I]alpha-bungarotoxin [( 125I]alpha-BGT) to localize within the chemosensory tissue the possible sites of action of exogenous and endogenous nicotinic cholinergic substances. In vitro equilibrium binding studies of intact carotid bodies determined a Kd of 5.57 nM and a Bmax of 9.21 pmol/g of tissue. Chronic section (12-15 days) of the carotid sinus nerve (CSN) did not change the amount of displaceable toxin binding. In contrast, the specific binding was reduced by 46% following removal of the superior cervical ganglion. Light microscope autoradiography of normal, CSN-denervated and sympathectomized carotid bodies revealed displaceable binding sites concentrated in lobules of type I and type II cells. Treatment of carotid bodies with 50 nM alpha-BGT in vitro reduced by 50% the release of [3H]dopamine (synthesized from [3H]tyrosine) caused by hypoxia or nicotine, and also significantly reduced the stimulus-evoked discharges recorded from the CSN. The data suggest an absence of alpha-BGT binding sites on the afferent terminals of the CSN and that nicotinic receptors located with parenchymal cell lobules may modulate the release of catecholamines from these cells.
D000818:Animals; D001345:Autoradiography; D002038:Bungarotoxins / Q000378:metabolism; D002344:Carotid Body / Q000378:metabolism*; D002415:Cats; D003714:Denervation; D004298:Dopamine / Q000378:metabolism; D005260:Female; D007700:Kinetics; D008297:Male; D011978:Receptors, Nicotinic / Q000378:metabolism*; D013562:Sympathectomy
D002038:Bungarotoxins; D011978:Receptors, Nicotinic; D004298:Dopamine