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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

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