Effect of low O2 on glucose uptake in rabbit carotid body

Abstract

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.