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J Appl Physiol 96: 376-383, 2004. First published August 15, 2003; doi:10.1152/japplphysiol.00726.2003
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HIGHLIGHTED TOPICS
Oxygen Sensing in Health and Disease

Acetylcholine release from the carotid body by hypoxia: evidence for the involvement of autoinhibitory receptors

Dong-Kyu Kim,1 Nanduri R. Prabhakar,2 and Ganesh K. Kumar1

Departments of 1Biochemistry and 2Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106

Submitted 14 July 2003 ; accepted in final form 1 August 2003

The purpose of the present study was to investigate whether hypoxia influences acetylcholine (ACh) release from the rabbit carotid body and, if so, to determine the mechanism(s) associated with this response. ACh is expressed in the rabbit carotid body (5.6 ± 1.3 pmol/carotid body) as evidenced by electrochemical analysis. Immunocytochemical analysis of the primary cultures of the carotid body with antibody specific to ACh further showed that ACh-like immunoreactivity is localized to many glomus cells. The effect of hypoxia on ACh release was examined in ex vivo carotid bodies harvested from anesthetized rabbits. The basal release of ACh during normoxia (~150 Torr) averaged 5.9 ± 0.5 fmol·min-1·carotid body-1. Lowering the PO2 to 90 and 20 Torr progressively decreased ACh release by ~15 and ~68%, respectively. ACh release returned to the basal value on reoxygenation. Simultaneous monitoring of dopamine showed a sixfold increase in dopamine release during hypoxia. Hypercapnia (21% O2 + 10% CO2) as well as high K+ (100 mM) facilitated ACh release from the carotid body, suggesting that hypoxia-induced inhibition of ACh release is not due to deterioration of the carotid body. Hypoxia had no significant effect on acetylcholinesterase activity in the medium, implying that increased hydrolysis of ACh does not account for hypoxia-induced inhibition of ACh release. In the presence of either atropine (10 µM) or domperidone (10 µM), hypoxia stimulated ACh release. These results demonstrate that glomus cells of the rabbit carotid body express ACh and that hypoxia overall inhibits ACh release via activation of muscarinic and dopaminergic autoinhibitory receptors in the carotid body.

hypercapnia; muscarinic receptors; dopaminergic receptors; glomus cells


Address for reprint requests and other correspondence: G. K. Kumar, Dept. of Biochemistry, School of Medicine, Case Western Reserve Univ., 10900 Euclid Ave., Cleveland, OH 44106-4935 (E-mail: kgk{at}po.cwru.edu).




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