{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T14:26:01Z","timestamp":1784816761175,"version":"3.55.0"},"reference-count":54,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2004,1]]},"abstract":"<jats:p> 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 \u00b1 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 (\u223c150 Torr) averaged 5.9 \u00b1 0.5 fmol\u00b7min<jats:sup>-1<\/jats:sup>\u00b7carotid body<jats:sup>-1<\/jats:sup>. Lowering the Po<jats:sub>2<\/jats:sub> to 90 and 20 Torr progressively decreased ACh release by \u223c15 and \u223c68%, 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% O<jats:sub>2<\/jats:sub> + 10% CO<jats:sub>2<\/jats:sub>) as well as high K<jats:sup>+<\/jats:sup> (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 \u03bcM) or domperidone (10 \u03bcM), 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. <\/jats:p>","DOI":"10.1152\/japplphysiol.00726.2003","type":"journal-article","created":{"date-parts":[[2004,1,31]],"date-time":"2004-01-31T00:57:54Z","timestamp":1075510674000},"page":"376-383","source":"Crossref","is-referenced-by-count":52,"title":["Acetylcholine release from the carotid body by hypoxia: evidence for the involvement of autoinhibitory receptors"],"prefix":"10.1152","volume":"96","author":[{"given":"Dong-Kyu","family":"Kim","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nanduri R.","family":"Prabhakar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ganesh K.","family":"Kumar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1042\/bj2160011"},{"key":"REF2","unstructured":"Baghdoyan HA, Lydic R, and Fleegal MA. 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