Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/43253
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Type: Journal article
Title: Activation of 5-HT1A receptors attenuates tachycardia induced by restraint stress in rats
Author: Ngampramuan, S.
Baumert, M.
Beig, M.
Kotchabhakdi, N.
Nalivaiko, E.
Citation: American Journal of Physiology-Regulatory Integrative and Comparative Physiology, 2008; 294(1):R132-R141
Publisher: Amer Physiological Soc
Issue Date: 2008
ISSN: 0363-6119
1522-1490
Statement of
Responsibility: 
Sukonthar Ngampramuan, Mathias Baumert, Mirza Irfan Beig, Naiphinich Kotchabhakdi, and Eugene Nalivaiko
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.
Keywords: serotonin; psychological stress; heart rate; sympathetic; medullary raphe
Rights: Copyright © 2008 by the American Physiological Society.
RMID: 0020075038
DOI: 10.1152/ajpregu.00464.2007
Appears in Collections:Electrical and Electronic Engineering publications

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