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This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 100/6/1902    most recent 01414.2005v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map 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 Montero, S. Articles by de Alvarez-Buylla, E. R. Search for Related Content PubMed PubMed Citation Articles by Montero, S. Articles by de Alvarez-Buylla, E. R.

Arginine-vasopressin mediates central and peripheral glucose regulation in response to carotid body receptor stimulation with Na-cyanide

Sergio Montero,^1,2 Herón Mendoza,³ Victoria Valles,⁴ Mónica Lemus,¹ Ramón Alvarez-Buylla,^1, and Elena R. de Alvarez-Buylla¹

¹Centro Universitario de Investigationes Biomedicas and ²Faculty of Medicine, University of Colima, Colima; ³Faculty of Medicine, Autonomous University of Tamaulipas, Tampico; and ⁴Department of Diabetes, National Institute of Medical Sciences and Nutrition "Salvador Zubirán," Mexico, Mexico

Submitted 8 November 2005 ; accepted in final form 13 February 2006

Hypoxic stimulation of the carotid body receptors (CBR) results in a rapid hyperglycemia with an increase in brain glucose retention. Previous work indicates that neurohypophysectomy inhibits this hyperglycemic response. Here, we show that systemic arginine vasopressin (AVP) induced a transient, but significant, increase in blood glucose levels and increased brain glucose retention, a response similar to that observed after CBR stimulation. Comparable results were obtained after intracerebral infusion of AVP. Systemic AVP-induced changes were maintained in hypophysectomized rats but were not observed after adrenalectomy. Glycemic changes after CBR stimulation were inhibited by pharmacological blockage of AVP V1a receptors with a V1a-selective receptor antagonist ([-Mercapto-,-cyclopentamethylenepropionyl¹,O-me-Tyr², Arg⁸]-vasopressin). Importantly, local application of micro-doses of this antagonist to the liver was sufficient to abolish the hyperglycemic response after CBR stimulation. These results suggest that AVP is a mediator of the hyperglycemic reflex and cerebral glucose retention following CBR stimulation. We propose that hepatic activation of AVP V1a receptors is essential for this hyperglycemic response.

chemoreceptors; central nervous system respiration