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This Article Full Text Full Text (PDF) All Versions of this Article: 585/3/721    most recent jphysiol.2007.144261v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Conde, S. V. Articles by Gonzalez, C. Search for Related Content PubMed PubMed Citation Articles by Conde, S. V. Articles by Gonzalez, C. Related Collections Cellular

¹ Ciber Enfermedades Respiratorias, Departamento de Bioquímica y Biología Moleculary Fisiología/Instituto de Biologíay Genética Molecular, Universidad de Valladolid/Consejo Superior de Investigaciones Científicas, Facultad de Medicina, 47005 Valladolid, Spain
² Department of Pharmacology, Faculty of Medical Sciences, New University of Lisbon, 1169-056 Lisbon, Portugal

Glucose deprivation (hypoglycaemia) is counterbalanced by a neuroendocrine response in order to induce fast delivery of glucose to blood. Some central neurons can sense glucose, but nevertheless the most important glucose sensors/glycaemia regulators are located outside the brain. Some recent experimental evidence obtained in carotid body (CB) slices and isolated chemoreceptor cells in culture supports a role for the CB in glucose sensing and presumably glucose homeostasis, but this role has been questioned on the basis of a lack of effect of low glucose on the carotid sinus nerve activity. This work was performed in an attempt to clarify if low glucose is or is not a stimulus for the rat CB chemoreceptors. Using freshly isolated intact CB preparations we have monitored the release of catecholamines (CAs) and ATP from chemoreceptor cells in response to several concentrations of glucose, as indices of chemoreceptor cell sensitivity to glycaemia, and the electrical activity in the carotid sinus nerve (CSN), as an index of reflex-triggering output of the CB. We have observed that basal (20% O₂) and hypoxia (7 and 10% O₂)-evoked release of CAs was identical in the presence of normal (5.55 mM) and low (3, 1 and 0 mM) glucose concentrations. 0 mM glucose did not activate the release of ATP from the CB, while hypoxia (5% O₂) did. Basal and hypoxia (5% O₂)-induced CSN action potential frequency was identical with 5.55 and 1 mM glucose. Our results indicate that low glucose is not a direct stimulus for the rat carotid body chemoreceptors.

(Received 31 August 2007; accepted after revision 15 October 2007; first published online 18 October 2007)
Corresponding author C. Gonzalez: Departamento de Bioquímica y, Biología Molecular y Fisiología, Facultad de Medicina. Universidad de Valladolid, 47005 Valladolid. Spain. Email: constanc{at}ibgm.uva.es