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https://hdl.handle.net/2440/43253
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dc.contributor.author | Ngampramuan, S. | - |
dc.contributor.author | Baumert, M. | - |
dc.contributor.author | Beig, M. | - |
dc.contributor.author | Kotchabhakdi, N. | - |
dc.contributor.author | Nalivaiko, E. | - |
dc.date.issued | 2008 | - |
dc.identifier.citation | American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, 2008; 294(1):R132-R141 | - |
dc.identifier.issn | 0363-6119 | - |
dc.identifier.issn | 1522-1490 | - |
dc.identifier.uri | http://hdl.handle.net/2440/43253 | - |
dc.description.abstract | To 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. | - |
dc.description.statementofresponsibility | Sukonthar Ngampramuan, Mathias Baumert, Mirza Irfan Beig, Naiphinich Kotchabhakdi, and Eugene Nalivaiko | - |
dc.language.iso | en | - |
dc.publisher | Amer Physiological Soc | - |
dc.rights | Copyright © 2008 by the American Physiological Society. | - |
dc.source.uri | http://dx.doi.org/10.1152/ajpregu.00464.2007 | - |
dc.subject | serotonin | - |
dc.subject | psychological stress | - |
dc.subject | heart rate | - |
dc.subject | sympathetic | - |
dc.subject | medullary raphe | - |
dc.title | Activation of 5-HT1A receptors attenuates tachycardia induced by restraint stress in rats | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1152/ajpregu.00464.2007 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Baumert, M. [0000-0003-2984-2167] | - |
Appears in Collections: | Aurora harvest 6 Electrical and Electronic Engineering publications |
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