Sukonthar NgampramuanMathias BaumertMirza Irfan BeigNaiphinich KotchabhakdiEugene NalivaikoThe Institute of Science and Technology for Research and Development, Mahidol UniversityUniversity of AdelaideFlinders UniversityFlinders Medical Centre2018-07-122018-07-122008-01-01American Journal of Physiology - Regulatory Integrative and Comparative Physiology. Vol.294, No.1 (2008)15221490036361192-s2.0-38149008742https://repository.li.mahidol.ac.th/handle/123456789/19006To 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-HT1Aantagonist 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-HT1Areceptors 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-HT1Areceptors attenuates this tachycardia by suppressing autonomic effects. At least some of the relevant receptors are located in the medullary rapheparapyramidal area. Copyright © 2008 the American Physiological Society.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.1152/ajpregu.00464.2007