{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T20:44:18Z","timestamp":1771533858133,"version":"3.50.1"},"reference-count":116,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,6,19]],"date-time":"2006-06-19T00:00:00Z","timestamp":1150675200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2006,7]]},"abstract":"<jats:p>All cells respond to metabolic stress. However, a variety of specialized cells, commonly referred to as O<jats:sub>2<\/jats:sub>\u2010sensing cells, are acutely sensitive to relatively small changes in <jats:styled-content><jats:italic>P<\/jats:italic><jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/tex2gif-sub-4.gif\" xlink:title=\"urn:x-wiley:00223751:media:TJP1588:tex2gif-sub-4\"\/><\/jats:styled-content>. Within a variety of organisms such O<jats:sub>2<\/jats:sub>\u2010sensing cells have evolved as vital homeostatic mechanisms that monitor O<jats:sub>2<\/jats:sub> supply and alter respiratory and circulatory function, as well as the capacity of the blood to transport O<jats:sub>2<\/jats:sub>. Thereby, arterial <jats:styled-content><jats:italic>P<\/jats:italic><jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/tex2gif-sub-9.gif\" xlink:title=\"urn:x-wiley:00223751:media:TJP1588:tex2gif-sub-9\"\/><\/jats:styled-content> may be maintained within physiological limits. In mammals, for example, two key tissues that contribute to this process are the pulmonary arteries and the carotid bodies. Constriction of pulmonary arteries by hypoxia optimizes ventilation\u2013perfusion matching in the lung, whilst carotid body excitation by hypoxia initiates corrective changes in breathing patterns via increased sensory afferent discharge to the brain stem. Despite extensive investigation, the precise mechanism(s) by which hypoxia mediates these responses has remained elusive. It is clear, however, that hypoxia inhibits mitochondrial function in O<jats:sub>2<\/jats:sub>\u2010sensing cells over a range of <jats:styled-content><jats:italic>P<\/jats:italic><jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/tex2gif-sub-12.gif\" xlink:title=\"urn:x-wiley:00223751:media:TJP1588:tex2gif-sub-12\"\/><\/jats:styled-content> that has no such effect on other cell types. This raised the possibility that AMP\u2010activated protein kinase might function to couple mitochondrial oxidative phosphorylation to Ca<jats:sup>2+<\/jats:sup> signalling mechanisms in O<jats:sub>2<\/jats:sub>\u2010sensing cells and thereby underpin pulmonary artery constriction and carotid body excitation by hypoxia. Our recent investigations have provided significant evidence in support of this view.<\/jats:p>","DOI":"10.1113\/jphysiol.2006.108381","type":"journal-article","created":{"date-parts":[[2006,5,19]],"date-time":"2006-05-19T00:43:23Z","timestamp":1147999403000},"page":"113-123","source":"Crossref","is-referenced-by-count":45,"title":["AMP\u2010activated protein kinase and the regulation of Ca<sup>2+<\/sup> signalling in O<sub>2<\/sub>\u2010sensing cells"],"prefix":"10.1113","volume":"574","author":[{"given":"A. 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