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The present experiments examined the effects of CH (9\u201316 days at 380 Torr) on the expression of P2X<jats:sub>2<\/jats:sub>purinoceptors in carotid body and chemoafferent neurons, as well as the effectiveness of P2X<jats:sub>2<\/jats:sub>receptor blocking drugs on CSN activity evoked by hypoxia. In the normal carotid body, immunocytochemical studies demonstrated a dense plexus of P2X<jats:sub>2<\/jats:sub>-positive nerve fibers penetrating lobules of type I cells. In addition, type I cells were lightly stained, indicating P2X<jats:sub>2<\/jats:sub>receptor expression. After CH, the intensity of P2X<jats:sub>2<\/jats:sub>receptor immunostaining was maintained in chemosensory type I cells and in the soma of chemoafferent neurons. P2 receptor expression on type I cells was confirmed by demonstrations of ATP-evoked increased intracellular Ca<jats:sup>2+<\/jats:sup>; this response was modulated by simultaneous exposure to hypoxia. In normal preparations, CSN activity evoked by hypoxia in vitro was 65% inhibited in the presence of specific P2X<jats:sub>2<\/jats:sub>receptor antagonists. However, unlike the absence of mecamylamine action after CH, P2X<jats:sub>2<\/jats:sub>antagonists remained effective against hypoxia-evoked activity after CH. Our findings indicate that ATP acting at P2X<jats:sub>2<\/jats:sub>receptors contributes to adjusted chemoreceptor activity after CH, indicating a possible role for purinergic mechanisms in the adaptation of the carotid body in a chronic low-O<jats:sub>2<\/jats:sub>environment.<\/jats:p>","DOI":"10.1152\/japplphysiol.00859.2005","type":"journal-article","created":{"date-parts":[[2005,12,15]],"date-time":"2005-12-15T23:41:11Z","timestamp":1134690071000},"page":"157-162","source":"Crossref","is-referenced-by-count":42,"title":["Effect of chronic hypoxia on purinergic synaptic transmission in rat carotid body"],"prefix":"10.1152","volume":"100","author":[{"given":"L.","family":"He","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B.","family":"Dinger","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"Stensaas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Fidone","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"R1","unstructured":"Almaraz L, Wang ZZ, Dinger B, and Fidone SJ.Neurotransmitter mediation of carotid chemoreceptor efferent inhibition. 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