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This Article Full Text Full Text (PDF) All Versions of this Article: 290/6/R1654    most recent 00704.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Zhang, W. Articles by Kuwaki, T. Search for Related Content PubMed PubMed Citation Articles by Zhang, W. Articles by Kuwaki, T.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Orexin neuron-mediated skeletal muscle vasodilation and shift of baroreflex during defense response in mice

Departments of ¹Molecular and Integrative Physiology and ⁴Autonomic Physiology, Chiba University Graduate School of Medicine, Chiba-City, Chiba; ²Department of Molecular Pharmacology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba; and ³Exploratory Research for Advanced Technology Yanagisawa Orphan Project, Japan Science and Technology Corporation, Tokyo, Japan

Submitted 3 October 2005 ; accepted in final form 9 January 2006

We have previously shown that some features of the defense response, such as increases in arterial blood pressure (AP), heart rate (HR), and ventilation were attenuated in prepro-orexin knockout (ORX-KO) mice. Here, we examined whether the same was true in orexin neuron-ablated [orexin/ataxin-3 transgenic mice (ORX/ATX-Tg)] mice. In addition, we examined other features of the defense response: skeletal muscular vasodilation and shift of baroreceptor reflex. In both anesthetized and conscious conditions, basal AP in ORX/ATX-Tg mice was significantly lower by 20 mmHg than in wild-type (WT) controls, as was the case in ORX-KO mice. The difference in AP disappeared after treatment with an -blocker but not with a -blocker, indicating lower sympathetic vasoconstrictor outflow. Stimulation of the perifornical area (PFA) in urethane-anesthetized ORX/ATX-Tg mice elicited smaller and shorter-lasting increases in AP, HR, and ventilation, and skeletal muscle vasodilation than in WT controls. In addition, air jet stress-induced elevations of AP and HR were attenuated in conscious ORX/ATX-Tg mice. After pretreatment with a -blocker, atenolol, stimulation of PFA suppressed phenylephrine (50 µg/kg iv)-induced bradycardia (HR = –360 ± 29 beats/min without PFA stimulation vs. –166 ± 26 during stimulation) in WT. This demonstrated the resetting of the baroreflex. In ORX/ATX-Tg mice, however, no significant suppression was observed (–355 ± 16 without stimulation vs. –300 ± 30 during stimulation). The present study provided further support for our hypothesis that orexin-containing neurons in PFA play a role as a master switch to activate multiple efferent pathways of the defense response and also operate as a regulator of basal AP.

hypothalamus; stress; blood pressure; respiration

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