Effect of low O2 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-[3H]deoxy-glucose. The rate of glucose consumption measured in 100% O2-equilibrated modified Tyrode medium was 61 nmol.g tissue-1 x 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% increase in the rate of glucose consumption. The glucose consumption of the nodose ganglion was not affected during similar incubation with low-O2 medium. High-resolution autoradiography of freeze-dried tissues revealed that the type I parenchymal cells are the principal site of glucose consumption in both 100% O2- and 20% O2-incubated carotid bodies. This metabolic response of the carotid body to hypoxia was not secondary to neurotransmitter release, because similar elevations in glucose utilization were observed with low-O2 medium containing zero Ca2+, a condition in which the release of neurotransmitters from type I cells is 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 carotid 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 in 100% O2-equilibrated solution and abolished the metabolic response produced by low-O2 medium. The results suggest that the utilization of metabolic energy is an integral component of the chemoreceptor response to hypoxia.