Submitted on November 8, 2005
Accepted on February 13, 2006
Arginine-vasopressin mediates central and peripheral glucose regulation in response to carotid body receptors stimulation with Na-cyanide
Sergio A. Montero1, Heron Mendoza2, Victoria Valles3, Monica Lemus4, Ramon Alvarez-Buylla, and Elena R. de Alvarez-Buylla4*
1 University Center for Biomedical Studies, University of Colima, Colima, Colima, Mexico; Faculty of Medicine, University of Colima, Colima, Colima, Mexico
2 Faculty of Medicine, Autonomous University of Tamaulipas, Tampico, Tamaulipas, Mexico
3 Department of Diabetes, National Institute of Medical Sciences and Nutrition, Mexico, D.F., Mexico
4 University Center for Biomedical Studies, University of Colima, Colima, Colima, Mexico
* To whom correspondence should be addressed. E-mail: rab{at}cgic.ucol.mx.
Hypoxic stimulation of the carotid body receptors (CBR) results in a rapid hyperglycemia with an increase in brain glucose retention. 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 were 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.
