- 作者: T.M. Wong J. Shan
- 作者服務機構: Department of Physiology, Faculty of Medicine, The University of Hong Kong, Hong Kong
- 中文摘要: --
- 英文摘要: The sympathetic nervous system, the most importantextrinsic regulatory mechanism of the heart, is inhibitedpostsynaptically and presynaptically by opioid peptidesproduced in the heart via their respective receptors. Thecardiac actions of β-adrenergic receptor (β-AR) stimula-tion 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 adenylylcyclase of the β-AR pathway by the pertussis toxin-sensi-tive G protein of the opioid pathway. Alterations in cross-talk between these two receptors occur in pathologicalsituations to meet bodily needs. In myocardial ischemia, when the sympathetic activity is increased, the inhibitionof β-AR stimulation by -opioid stimulation is also en-hanced, thus reducing the workload, oxygen consump-tion and cardiac injury. Whereas cardiac responsivenessto sympathetic discharges is also reduced after chronichypoxia, the cross-talk between -OR and β-AR is re-duced to prevent undue suppression of the sympatheticinfluence on the heart. On the other hand, impairment ofthe cross-talk may result in abnormality. A lack or a sig-nificant reduction in the inhibition of β-AR stimulation by -OR stimulation may lead to an excessive increase incardiac activities, which contribute to the maintenance ofhigh arterial blood pressure in spontaneously hyperten-sive rats. Other than opioid peptides, female sex hor-mone and adenosine also inhibit the sympathetic actionson the heart. In addition, sympathetic action is also inhib-ited presynaptically by -opioid peptides via their recep-tor.
- 中文關鍵字: --
- 英文關鍵字: Adrenergic receptor. Opioid receptor. Heart Sympathetic nervous system. Female sex hormone. Adenosine. Inhibition