Characterization of [3H]U69593 binding sites in the rat heart by receptor binding assays

Tai, Kwok-Keung; Jin, Wen-Qiao; Chan, Tin-Yau; Wong, Tak‐Ming

doi:10.1016/0022-2828(91)90086-2

Cited by 57 publications

(27 citation statements)

References 10 publications

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“…Morphine has been shown to act on the heart via both Î-and ‰-ORs [6], which are the ORs present in the heart [32,34]. These two types of receptors have been shown to mediate cardioprotection of ischemic preconditioning [35].…”

Section: Discussionmentioning

confidence: 99%

“…It is well known that both Î- [32,34] and ‰-ORs [34] exist in the heart. It has been demonstrated that cardioprotection of ischemic preconditioning was abolished by blockade of Î-or ‰-, but not Ì-ORs [35], indicating that only Î-and ‰-ORs mediate cardioprotection of ischemic preconditioning.…”

Section: Discussionmentioning

confidence: 99%

“…The roles of the two other OR subtypes, Î-OR, which is present in the heart and known to mediate both immediate [11,35] and delayed [3,36,37,39] cardioprotection of preconditioning, and Ì-OR, which has not been found to be present in the heart [15,32,34], are not known.…”

Section: Introductionmentioning

confidence: 99%

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Role of Opioid Receptors in Cardioprotection of Cold-Restraint Stress and Morphine

Wu¹,

Wong²,

Chen³

et al. 2004

J Biomed Sci

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Since cold exposure confers cardioprotection, the present study attempted to determine the role of opioid receptors (OR). Stress with cold exposure and restraint for 3 h, shown previously to induce peptic ulcer in a synergistic manner, attenuated infarct size induced by myocardial ischemia and reperfusion in the isolated perfused rat heart from 36.64 ± 1.8 to 22.85 ± 2.6%. This is similar to protecting the rat with morphine at 8 mg/kg, which also attenuated the infarct size from 36.26 ± 1.6 to 20.30 ± 2.1%. The effects of cold-restraint or morphine were abolished by naloxone, a non-selective OR antagonist; nor-binaltorphimine, a selective ĸ-OR antagonist; naltrindole, a selective δ-OR antagonist, or CTOP, a selective µ-OR antagonist. The effects were also attenuated by blockade of protein kinase C or the mitochondrial K_ATP channel. The finding is first evidence that all three OR subtypes mediate cardioprotection of cold-restraint stress in the rat.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Role of Opioid Receptors in Cardioprotection of Cold-Restraint Stress and Morphine

Wu¹,

Wong²,

Chen³

et al. 2004

J Biomed Sci

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“…Receptor binding studies show that there are ‰- [2,17,43] and Î- [2,17,41,43], but not Ì-OR [17] binding sites in the heart. In a subsequent study [16], it was found that Ì-receptor binding sites are only present in the left atrium of the rat.…”

Section: Cardiac Opioid Peptides and Receptorsmentioning

confidence: 99%

Modulation of Sympathetic Actions on the Heart by Opioid Receptor Stimulation

Wong

Shan

2001

Journal of Biomedical Science

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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.

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“…It should be noted that although 5-receptor binding sites were shown to be present in the heart, only k-receptor binding was reported to be present in the heaft by all groups. Further study with a displacement method demon strated that the binding of [3H]-U69593, a selective k-agonist, was effectively displaced by selective kr agonists, U69593 and U50488H, but only weakly by a selective k2-agonist, Met5-enkephalin-Arg6-Phe7 [4], In addition, there was no binding site for the [3H]-etorphin, which binds to a k2, but not kisite [4]. The results suggest that k| binding sites are predominant in the heart.…”

Section: Introductionmentioning

confidence: 99%

Signal Transduction in the Cardiac k-Receptor

Wong¹,

Sheng²,

Wong

et al. 1995

Neurosignals

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The presence of k-binding sites in the heart suggests a regulatory role of k-receptor in the cardiac functions. Recent studies have provided evidence that activation of cardiac k-receptor elevates intracellular free calcium ([Ca²⁺]i) by increasing mobilization of calcium from the intracellular store. The mobilization of intracellular calcium results from an increased production of inositol-1,4,5-trisphosphate (IP3). The increase in [Ca²⁺]i may manifest in cardiac arrhythmias while the depletion of calcium from the intracellular store may reduce the contractility elicited upon depolarization. The responses of IP₃/[Ca²⁺]i are significantly attenuated after development of tolerance to k-opioids due mainly to the impairment of postreceptor events. The attenuated responses of IP₃/[Ca²⁺]i to k-receptor activation may be responsible for the failure of the k-agonists to induce cardiac arrhythmias and to reduce electrically induced calcium transients in the ventricular myocytes.

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Characterization of [3H]U69593 binding sites in the rat heart by receptor binding assays

Cited by 57 publications

References 10 publications

Role of Opioid Receptors in Cardioprotection of Cold-Restraint Stress and Morphine

Role of Opioid Receptors in Cardioprotection of Cold-Restraint Stress and Morphine

Modulation of Sympathetic Actions on the Heart by Opioid Receptor Stimulation

Signal Transduction in the Cardiac k-Receptor

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