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Department of Physiology, University of Utah, Salt Lake City, Utah
Submitted 9 July 2004 ; accepted in final form 17 October 2004
Current views suggest that oxygen sensing in the carotid body occurs in chemosensory type I cells, which excite synaptically apposed chemoafferent nerve terminals in the carotid sinus nerve (CSN). Prolonged exposure in a low-oxygen environment [i.e., chronic hypoxia (CH)] elicits an elevated stimulus-evoked discharge in chemoreceptor CSN fibers (i.e., increased chemosensitivity). In the present study, we evaluated cholinergic chemotransmission in the rat carotid body in an effort to test the hypothesis that CH enhances ACh-mediated synaptic activity between type I cells and chemoafferent nerve terminals. Animals were exposed in a hypobaric chamber (barometric pressure = 380 Torr) for 9–22 days before evaluation of chemoreceptor activity using an in vitro carotid body/CSN preparation. Nerve activity evoked by ACh was significantly larger (P < 0.01) after CH, suggesting increased expression of cholinergic receptors. Approximately 80% of the CSN impulse activity elicited by ACh (100- or 1,000-µg bolus) in both normal and CH preparations was blocked by the specific nicotinic receptor antagonist mecamylamine (100 µM). CSN activity elicited by acute hypoxia or hypercapnia in normal preparations was likewise blocked (
80%) in the presence of 100 µM mecamylamine, but after CH the enhanced CSN activity elicited by acute hypoxia or hypercapnia was not reduced in the presence of 100 or 500 µM mecamylamine. A muscarinic receptor antagonist, atropine (10 µM), and a specific nicotinic receptor 
7 subunit antagonist, methyllycaconatine (50 nM), blocked 
50% of the hypoxia-evoked activity in normal preparations but were ineffective after CH. Prolonged exposure to hypoxia appears to dramatically alter chemotransmission in the carotid body, and may induce alternative neurotransmitter mechanisms and/or electrical coupling between type I cells and chemoafferent nerve terminals.
carotid sinus nerve; low-oxygen environment; acetylcholine; hypercapnia
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