Hypocretin/orexin type 1 receptor in brain: role in cardiovascular control and the neuroendocrine response to immobilization stress.

Full Abstract

Hypocretin/orexin acts pharmacologically in the hypothalamus to stimulate stress hormone secretion at least in part by an action in the hypothalamic paraventricular nucleus, where the peptide's receptors have been localized. In addition, orexin acts in the brain to increase sympathetic tone and, therefore, mean arterial pressure and heart rate. We provide evidence for the role of endogenously produced hypocretin/orexin in the physiological response to immobilization stress and identify the receptor subtype responsible for this action of the peptide. Antagonism of the orexin type 1 receptor (OX(1)R) in the brain prevented the ACTH-stimulating effect of centrally administered hypocretin/orexin. Furthermore, pretreatment of animals with the OX(1)R antagonist blocked the ACTH response to immobilization/restraint stress. The OX(1)R antagonist did not, however, block the pharmacological or physiological release of prolactin in these two models. Antagonism of the OX(1)R also blocked the central action of orexin to elevate mean arterial pressures and heart rates in conscious rats. These data suggest receptor subtype-selective responses to hypocretin/orexin and provide further evidence for the importance of endogenously produced peptide in the physiological control of stress hormone secretion.

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Author information

Author/s: Samson, Willis K (WK); Bagley, Sara L (SL); Ferguson, Alastair V (AV); White, Meghan M (MM);

Affiliation: Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, St. Louis, MO 63104, USA. samsonwk(-atsign-)slu.edu

Grants: HL-68652 (Agency:NHLBI NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural

Journal: American journal of physiology. Regulatory, integrative and comparative physiology (Am J Physiol Regul Integr Comp Physiol), published in United States. (Language: eng)

Reference: 2007-Jan; vol 292 (issue 1) : pp R382-7

Dates: Created 2007/01/01; Completed 2007/02/08; Revised 2008/11/21;

PMID: 16902182, status: MEDLINE (last retrieval date: 12/26/2008)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Adrenocorticotropic Hormone - blood
Animals
Blood Pressure - drug effects; physiology
Brain - physiology
Cardiovascular Physiological Phenomena
Heart Rate - drug effects; physiology
Hypothalamus - drug effects; physiology
Injections, Intraventricular
Intracellular Signaling Peptides and Proteins - pharmacology
Male

Male
Neuropeptides - pharmacology
Neurosecretory Systems - physiopathology
Prolactin - blood
Rats
Rats, Sprague-Dawley
Receptors, G-Protein-Coupled - antagonists & inhibitors; physiology
Receptors, Neuropeptide - antagonists & inhibitors; physiology
Restraint, Physical
Stress, Psychological - physiopathology

Associated Chemicals: Intracellular Signaling Peptides and Proteins (0) ; Neuropeptides (0) ; Receptors, G-Protein-Coupled (0) ; Receptors, Neuropeptide (0) ; orexin receptors (0) ; orexins (0) ; Adrenocorticotropic Hormone (9002-60-2) ; Prolactin (9002-62-4)

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