Arginine-vasopressin in nucleus of the tractus solitarius induces hyperglycemia and brain glucose retention

Yarkov, A; Montero, S; Lemus, M; de Alvarez-Buylla, ER; Alvarez-Buylla, R

Abstract

Hypothalamic arginine-vasopressin (AVP) plays an important role both as a neurotransmitter and hormone in the regulation of blood glucose and feeding behavior. AVP-containing axons from the parvocellular subdivision of paraventricular nucleus of the hypothalamus terminate in the nucleus of the tractus solitarius (NTS), but the Function of this projection is not known. Interestingly, the NTS also receives afferent information from the carotid body and other peripheral receptors involved in glucose homeostasis. We have previously reported that stimulation of the carotid body receptors initiates a hyperglycemic reflex and increases brain glucose retention. Here we show that direct administration of micro-doses of AVP into the NTS of anesthetized or awake rats rapidly increased the levels of blood glucose concentration and brain arterio-venous (A-V) glucose difference. This effect was not observed when the same doses of AVP were injected in the brainstem outside NTS. Arginine-vasopressin antagonist microinjections alone produced a small but significant reduction in brain A-V glucose. Pre-administered VPI-receptor antagonist [beta -mercapto-beta,beta -cyclopenramethylene-propl(1) ,O-Me-Tyr(2),Arg(8)]vasopressin blocked the effects of AVP. These results indicate that AVP acting on its receptors locally within the NTS participates in glucose homeostasis, increasing both blood glucose concentration and brain A-V glucose differences. Hypothalamic AVP may facilitate hyperglycemic responses initiated by peripheral signals processed at the level of the NTS. (C) 2001 Published by Elsevier Science B.V.

Más información

Título según WOS: ID WOS:000169092200010 Not found in local WOS DB
Título de la Revista: BRAIN RESEARCH
Volumen: 902
Número: 2
Editorial: ELSEVIER SCIENCE BV
Fecha de publicación: 2001
Página de inicio: 212
Página final: 222
DOI:

10.1016/S0006-8993(01)02404-0

Notas: ISI