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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

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

¹Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, St. Louis, Missouri; and ²Department of Physiology, Queen's University, Kingston, Ontario, Canada

Submitted 13 July 2006 ; accepted in final form 9 August 2006

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 (OX₁R) in the brain prevented the ACTH-stimulating effect of centrally administered hypocretin/orexin. Furthermore, pretreatment of animals with the OX₁R antagonist blocked the ACTH response to immobilization/restraint stress. The OX₁R antagonist did not, however, block the pharmacological or physiological release of prolactin in these two models. Antagonism of the OX₁R 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.

autonomic function; hypothalamus; adrenocorticotropin; prolactin

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