Arginine-vasopressin mediates central and peripheral glucose regulation in response to carotid body receptor stimulation with Na-cyanide.
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 ([beta-Mercapto-beta,beta-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.
Montero
Sergio
S
CUIB, Universidad de Colima, Ave. 25 de Julio s/n, Colima, Col. 28045, México. checo@cgic.ucol.mx
Mendoza
Herón
H
Valles
Victoria
V
Lemus
Mónica
M
Alvarez-Buylla
Ramón
R
de Alvarez-Buylla
Elena R
ER
D000311:Adrenal Glands / Q000502:physiology; D000315:Adrenalectomy; D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin / Q000502:physiology*; D001923:Brain Chemistry; D002344:Carotid Body / Q000737:chemistry / Q000502:physiology*; D002395:Catecholamines / Q000378:metabolism; D002628:Chemoreceptor Cells / Q000187:drug effects* / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005934:Glucagon / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006943:Hyperglycemia / Q000139:chemically induced / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D017483:Receptors, Vasopressin / Q000502:physiology; D012966:Sodium Cyanide / Q000494:pharmacology*; D014667:Vasopressins / Q000494:pharmacology
D065092:Antidiuretic Hormone Receptor Antagonists; D002395:Catecholamines; D004791:Enzyme Inhibitors; D017483:Receptors, Vasopressin; D014667:Vasopressins; D001127:Arginine Vasopressin; C066604:oxytocin, beta-mercapto-beta,beta-cyclopentamethylenepropionic acid-Trp(2)-Phe(3)-Ile(4)-Arg(8)-; D005934:Glucagon; D005947:Glucose; D012966:Sodium Cyanide