The effects of low O2 on glucose consumption in the rabbit carotid body were studied using the in vitro 2-deoxyglucose technique. Metabolically active structures within the tissue were localized autoradiographically after freeze-drying and vacuum fixation/embedding of selected incubated tissue samples. In 100% O2-equilibrated media, the mean basal glucose consumption calculated from the rate of 2-[1,2-3H]deoxy-D-glucose phosphorylation and its specific activity in the incubation media was 61 nmol.g tissue-1.min-1 in the carotid body and 42 nmol.g tissue-1.min-1 in parallel experiments with nodose ganglia. Low PO2 (20% O2-equilibrated media in vitro) increased glucose consumption in the carotid body by 44% but did not alter glucose metabolism of nodose ganglia. Autoradiographic data showed that preneural type I parenchymal cells are the principal site of glucose consumption in carotid chemosensory tissue. The mechanisms responsible for the hypoxia-induced increase in glucose consumption by the type I cells are discussed in relation to sensory transduction by the carotid body chemoreceptors.