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Hypoxia transduction by carotid body chemoreceptors in mice lacking dopamine D₂ receptors

¹Ciber Enfermedades Respiratorias, Departamento de Bioquímica y Biología Molecular y Fisiología, Instituto de Biología y Genética Molecular, Facultad de Medicina, Universidad de Valladolid, and Consejo Superior de Investigaciones Científicas (CSIC), Valladolid, Spain; ²Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut; and ³Instituto Cajal, CSIC, Madrid, Spain

Submitted 12 April 2007 ; accepted in final form 30 July 2007

Hypoxia-induced dopamine (DA) release from carotid body (CB) glomus cells and activation of postsynaptic D₂ receptors have been proposed to play an important role in the neurotransmission process between the glomus cells and afferent nerve endings. To better resolve the role of D₂ receptors, we examined afferent nerve activity, catecholamine content and release, and ventilation of genetically engineered mice lacking D₂ receptors (D₂^–/– mice). Single-unit afferent nerve activities of D₂^–/– mice in vitro were significantly reduced by 45% and 25% compared with wild-type (WT) mice during superfusion with saline equilibrated with mild hypoxia (PO₂ 50 Torr) or severe hypoxia (PO₂ 20 Torr), respectively. Catecholamine release in D₂^–/– mice was enhanced by 125% in mild hypoxia and 75% in severe hypoxia compared with WT mice, and the rate of rise was increased in D₂^–/– mice. We conclude that CB transduction of hypoxia is still present in D₂^–/– mice, but the response magnitude is reduced. However, the ventilatory response to acute hypoxia is maintained, perhaps because of an enhanced processing of chemoreceptor input by brain stem respiratory nuclei.

hypoxia sensing; arterial chemoreceptors; chemoreception