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Table of Contents
Vol. 8, No. 4, 2001
Issue release date: July–August 2001
Section title: Review
J Biomed Sci 2001;8:299–306
(DOI:10.1159/000054047)

Modulation of Sympathetic Actions on the Heart by Opioid Receptor Stimulation

Wong T.M. · Shan J.
Department of Physiology, Faculty of Medicine, The University of Hong Kong, Hong Kong

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Article / Publication Details

First-Page Preview
Abstract of Review

Published online: 7/6/2001

Number of Print Pages: 8
Number of Figures: 4
Number of Tables: 1

ISSN: 1021-7770 (Print)
eISSN: 1423-0127 (Online)

For additional information: http://www.karger.com/JBS

Abstract

The sympathetic nervous system, the most important extrinsic regulatory mechanism of the heart, is inhibited postsynaptically and presynaptically by opioid peptides produced in the heart via their respective receptors. The cardiac actions of β-adrenergic receptor (β-AR) stimulation are attenuated by activation of the opioid receptor (OR) with OR agonist at ineffective concentrations, implying cross-talk between the OR and β-AR. This cross-talk results from inhibition of the Gs protein and adenylyl cyclase of the β-AR pathway by the pertussis toxin-sensitive G protein of the opioid pathway. Alterations in cross-talk between these two receptors occur in pathological situations to meet bodily needs. In myocardial ischemia, when the sympathetic activity is increased, the inhibition of β-AR stimulation by ĸ-opioid stimulation is also enhanced, thus reducing the workload, oxygen consumption and cardiac injury. Whereas cardiac responsiveness to sympathetic discharges is also reduced after chronic hypoxia, the cross-talk between ĸ-OR and β-AR is reduced to prevent undue suppression of the sympathetic influence on the heart. On the other hand, impairment of the cross-talk may result in abnormality. A lack or a significant reduction in the inhibition of β-AR stimulation by ĸ-OR stimulation may lead to an excessive increase in cardiac activities, which contribute to the maintenance of high arterial blood pressure in spontaneously hypertensive rats. Other than opioid peptides, female sex hormone and adenosine also inhibit the sympathetic actions on the heart. In addition, sympathetic action is also inhibited presynaptically by ĸ-opioid peptides via their receptor.


  

Author Contacts

T.M. Wong, PhD
Department of Physiology
Faculty of Medicine, The University of Hong Kong
Sassoon Road (Hong Kong)
Tel. +852 2819 9194, Fax +852 2855 9730, E-Mail wongtakm@hkucc.hku.hk

  

Article Information

Received: Received: March 1, 2001
Acccepted: March 14, 2001
Number of Print Pages : 8
Number of Figures : 4, Number of Tables : 1, Number of References : 62

  

Publication Details

Journal of Biomedical Science (Sponsored by the National Science Council, Taipei)

Vol. 8, No. 4, Year 2001 (Cover Date: July-August 2001)

Journal Editor: S.H.H.Chan, Kaohsiung
ISSN: 1021–7770 (print), 1423–0127 (Online)

For additional information: http://www.karger.com/journals/jbs


Article / Publication Details

First-Page Preview
Abstract of Review

Published online: 7/6/2001

Number of Print Pages: 8
Number of Figures: 4
Number of Tables: 1

ISSN: 1021-7770 (Print)
eISSN: 1423-0127 (Online)

For additional information: http://www.karger.com/JBS


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