EFFECT OF LOW O-2 ON GLUCOSE-UPTAKE IN RABBIT CAROTID-BODY

Glucose consumption in the rabbit carotid body was studied in vitro by measuring phosphorylation rates of tracer concentrations of 2-[H-3]de oxyglucose. The rate of glucose consumption measured in 100% O2-equili brated modified Tyrode medium was 61 nmol . g tissue-1 . min-1 and was linear for up to 30 min. Incubation of carotid bodies for 5 or 10 min in moderately hypoxic solution (20% O2-80% N2) resulted in a 44% incr ease in the rate of glucose consumption. The glucose consumption of th e nodose ganglion was not affected during similar incubation with low- O2 medium. High-resolution autoradiography of freeze-dried tissues rev ealed that the type I parenchymal cells are the principal site of gluc ose consumption in both 100% O2- and 20% O2-incubated carotid bodies. This metabolic response of the carotid body to hypoxia was not seconda ry to neurotransmitter release, because similar elevations in glucose utilization were observed with low-O2 medium containing zero Ca2+, a c ondition in which the release of neurotransmitters from type I cells i s inhibited. Lowering the pH of the incubation medium from 7.4 to 7 or 6.8 markedly reduced the rate of glucose utilization by both the caro tid body and the nodose ganglion. Ouabain (2 x 10(-4) and 1 x 10(-3) M ) reduced by 20% the glucose consumption of carotid bodies incubated i n 100% O2-equilibrated solution and abolished the metabolic response p roduced by low-O2 medium. The results suggest that the utilization of metabolic energy is an integral component of the chemoreceptor respons e to hypoxia.