Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/43253
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dc.contributor.authorNgampramuan, S.en
dc.contributor.authorBaumert, M.en
dc.contributor.authorBeig, M.en
dc.contributor.authorKotchabhakdi, N.en
dc.contributor.authorNalivaiko, E.en
dc.date.issued2008en
dc.identifier.citationAmerican Journal of Physiology-Regulatory Integrative and Comparative Physiology, 2008; 294(1):R132-R141en
dc.identifier.issn0363-6119en
dc.identifier.issn1522-1490en
dc.identifier.urihttp://hdl.handle.net/2440/43253-
dc.description.abstractTo better understand the central mechanisms that mediate increases in heart rate (HR) during psychological stress, we examined the effects of systemic and intramedullary (raphe region) administration of the serotonin-1A (5-HT1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)tetraline (8-OH-DPAT) on cardiac changes elicited by restraint in hooded Wistar rats with preimplanted ECG telemetric transmitters. 8-OH-DPAT reduced basal HR from 356 ± 12 to 284 ± 12 beats/min, predominantly via a nonadrenergic, noncholinergic mechanism. Restraint stress caused tachycardia (an initial transient increase from 318 ± 3 to 492 ± 21 beats/min with a sustained component of 379 ± 12 beats/min). β-Adrenoreceptor blockade with atenolol suppressed the sustained component, whereas muscarinic blockade with methylscopolamine (50 µg/kg) abolished the initial transient increase, indicating that sympathetic activation and vagal withdrawal were responsible for the tachycardia. Systemic administration of 8-OH-DPAT (10, 30, and 100 µg/kg) attenuated stress-induced tachycardia in a dose-dependent manner, and this effect was suppressed by the 5-HT1A antagonist WAY-100635 (100 µg/kg). Given alone, the antagonist had no effect. Systemically injected 8-OH-DPAT (100 µg/kg) attenuated the sympathetically mediated sustained component (from +85 ± 19 to +32 ± 9 beats/min) and the vagally mediated transient (from +62 ± 5 to +25 ± 3 beats/min). Activation of 5-HT1A receptors in the medullary raphe by microinjection of 8-OH-DPAT mimicked the antitachycardic effect of the systemically administered drug but did not affect basal HR. We conclude that tachycardia induced by restraint stress is due to a sustained increase in cardiac sympathetic activity associated with a transient vagal withdrawal. Activation of central 5-HT1A receptors attenuates this tachycardia by suppressing autonomic effects. At least some of the relevant receptors are located in the medullary raphe-parapyramidal area.en
dc.description.statementofresponsibilitySukonthar Ngampramuan, Mathias Baumert, Mirza Irfan Beig, Naiphinich Kotchabhakdi, and Eugene Nalivaikoen
dc.language.isoenen
dc.publisherAmer Physiological Socen
dc.rightsCopyright © 2008 by the American Physiological Society.en
dc.subjectserotonin; psychological stress; heart rate; sympathetic; medullary rapheen
dc.titleActivation of 5-HT1A receptors attenuates tachycardia induced by restraint stress in ratsen
dc.typeJournal articleen
dc.identifier.rmid0020075038en
dc.identifier.doi10.1152/ajpregu.00464.2007en
dc.identifier.pubid45982-
pubs.library.collectionElectrical and Electronic Engineering publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
Appears in Collections:Electrical and Electronic Engineering publications

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