Wong T M, Shan J
Department of Physiology, Faculty of Medicine, The University of Hong Kong, Hong Kong.
J Biomed Sci. 2001 Jul-Aug;8(4):299-306. doi: 10.1007/BF02258370.
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 beta-adrenergic receptor (beta-AR) stimulation are attenuated by activation of the opioid receptor (OR) with OR agonist at ineffective concentrations, implying cross-talk between the OR and beta-AR. This cross-talk results from inhibition of the Gs protein and adenylyl cyclase of the beta-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 beta-AR stimulation by kappa-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 kappa-OR and beta-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 beta-AR stimulation by kappa-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 kappa-opioid peptides via their receptor.
交感神经系统是心脏最重要的外在调节机制，心脏产生的阿片肽通过其各自的受体在突触后和突触前对其产生抑制作用。在无效浓度下，用阿片受体（OR）激动剂激活阿片受体可减弱β-肾上腺素能受体（β-AR）刺激的心脏效应，这意味着OR和β-AR之间存在相互作用。这种相互作用是由阿片肽途径中对百日咳毒素敏感的G蛋白抑制β-AR途径中的Gs蛋白和腺苷酸环化酶所致。在病理情况下，这两种受体之间的相互作用会发生改变以满足身体需求。在心肌缺血时，当交感神经活动增强时，κ-阿片肽刺激对β-AR刺激的抑制作用也会增强，从而减少工作量、氧消耗和心脏损伤。而在慢性缺氧后，心脏对交感神经放电的反应性也会降低，κ-OR和β-AR之间的相互作用会减弱，以防止交感神经对心脏的影响受到过度抑制。另一方面，相互作用的受损可能会导致异常。κ-OR刺激对β-AR刺激的抑制作用缺乏或显著降低可能导致心脏活动过度增加，这有助于自发性高血压大鼠维持高动脉血压。除了阿片肽外，女性性激素和腺苷也会抑制交感神经对心脏的作用。此外，κ-阿片肽还通过其受体在突触前抑制交感神经作用。
