Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/43253
Citations | ||
Scopus | Web of Science® | Altmetric |
---|---|---|
?
|
?
|
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. |
DOI: | 10.1152/ajpregu.00464.2007 |
Published version: | http://dx.doi.org/10.1152/ajpregu.00464.2007 |
Appears in Collections: | Aurora harvest 6 Electrical and Electronic Engineering publications |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.