Journal of Applied Physiology AJP: Lung Cellular and Molecular Physiology
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J Appl Physiol 92: 975-981, 2002; doi:10.1152/japplphysiol.00852.2001
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Vol. 92, Issue 3, 975-981, March 2002

Central dopamine modulates anapyrexia but not hyperventilation induced by hypoxia

Renata C. H. Barros1 and Luiz G. S. Branco2

1 Departamento de Fisiologia, Faculdade de Medicina de Ribeirão Preto and, 2 Departamento de Morfologia, Estomatologia e Fisiologia, Faculdade de Odontologia de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil

Hypoxia causes hyperventilation and decreases body temperature (Tb) and metabolism [O2 consumption (VO2)]. Because dopamine (DA) is released centrally in response to peripheral chemoreceptor stimulation, we tested the hypothesis that central DA mediates the ventilatory, thermal, and metabolic responses to hypoxia. Thus we predicted that injection of haloperidol (a DA D2-receptor antagonist) into the third ventricle would augment hyperventilation and attenuate the drop in Tb and VO2 in conscious rats. We measured ventilation, Tb, and VO2 before and after intracerebroventricular injection of haloperidol or vehicle (5% DMSO in saline), followed by a 30-min period of hypoxia exposure. Haloperidol did not change Tb or VO2 during normoxia; however, breathing frequency was decreased. During hypoxia, haloperidol significantly attenuated the falls in Tb and VO2, although hyperventilation persisted. The present study shows that central DA participates in the thermal and metabolic responses to hypoxia without affecting hyperventilation, showing that DA is not a common mediator of this interaction.

haloperidol; ventilation; body temperature; metabolism; awake rats


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