Further characterization of [3H]U69593 binding sites in the rat heart

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

doi:10.1016/s0022-2828(95)90227-9

Cited by 25 publications

(12 citation statements)

References 19 publications

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“…The maximal number of left ventricular KOR specific binding sites is lower compared to the brain and spinal cord, and these KOR specific binding sites reveal a somewhat lower receptor affinity, although still in the nanomolar range. Consistently, KOR specific binding sites have been suggested in the atrium and ventricle of rats [29] and have been confirmed by others [30,31]. Only recently Theisen and his coworkers were able to translate those findings into healthy porcine myocardial tissue in which they detected KOR in all heart chambers by several different methods [11].…”

Section: Discussionsupporting

confidence: 61%

Upregulation of the kappa opioidergic system in left ventricular rat myocardium in response to volume overload

Treskatsch

Shaqura

Dehe

et al. 2015

Pharmacological Research

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Section: Discussionsupporting

confidence: 61%

Upregulation of the kappa opioidergic system in left ventricular rat myocardium in response to volume overload

Treskatsch

Shaqura

Dehe

et al. 2015

Pharmacological Research

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“…In rat isolated cardiomyocytes, Ventura and colleagues reported that both κ- and δ-, but not μ-selective radioligands exhibited a high affinity, suggesting the presence of δ- and κ-receptors in cardiomyocytes [12]. The κ-binding site, more specifically κ 1 , was reported in the crude membrane preparation of a rat heart homogenate [13], and both κ- and δ-, but not μ-receptors, have been identified in rat atrial and ventricular tissue [14]. Furthermore, opioid peptides were shown to have marked effects on cardiac muscle function in rat ventricular cardiomyocytes mediated by κ- and δ-receptor, but not μ-receptor stimulation [15].…”

Section: Opioid Receptorsmentioning

confidence: 99%

Opioid-induced Cardioprotection

Tanaka¹,

Kersten²,

Riess³

2014

CPD

104

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Ischemic heart disease and myocardial infarction continue to be leading causes of cardiovascular morbidity and mortality. Activation of opioid, adenosine, bradykinin, adrenergic and other G-protein coupled receptors have been found to be cardioprotective. κ- and/or δ-opioid receptor activation is involved in direct myocardial protection, while the role of μ-opioid receptors seems less clear. In addition, differential affinities to the three opioid-receptor subtypes by various agonists and cross-talk among different G-protein coupled receptors render conclusions regarding opioid-mediated cardioprotection challenging. The present review will focus on the protective effects of endogenously released opioid peptides as well as exogenously administered opioids such as morphine, fentanyl, remifentanil, butorphanol, and methadone against myocardial ischemia/reperfusion injury. Receptor heterodimerization and cross-talk as well as interactions with other cardioprotective techniques will be discussed. Implications for opioid-induced cardioprotection in humans and for future drug development to improve myocardial salvage will be provided.

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“…The discovery that the mammalian myocardial cells possess opioid receptors (Jin et al 1995;Steele et al 1996;Wegener and Kunmer 1994;Weihe et al 1985;Witer et al 1996) has led to studies aimed at investigating direct myocardial effects due to opioid receptor stimulation and identifying possible intracellular opioidergic pathways.…”

Section: Introductionmentioning

confidence: 99%

Catecholaminergic activity and 3',5'-cyclic adenosine monophosphate levels in heart right ventricle after naloxone induced withdrawal

Milanés

Fuente

Laorden

2000

Naunyn-Schmiedeberg's Arch Pharmacol

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This study evaluated the adaptive changes in noradrenergic neurons and the concomitant production of cAMP during morphine dependence and withdrawal in the right ventricle of the rat. Rats were made dependent on morphine by morphine pellet implantation for 7 days. On the day of sacrifice animals received an acute injection of saline or naloxone (1 mg/kg s.c.) and were decapitated 30 min later. Pretreatment with propranolol 15 min prior to naloxone was conducted to evaluate the possible implication of beta-adrenoceptors. The contents of noradrenaline and dopamine and their metabolites were examined. After naloxone administration to morphine-dependent rats (withdrawal) there was a pronounced increase in the content of normetanephrine and 3,4-dihydroxyphenylacetic acid and increased noradrenaline and dopamine turnover. In addition cAMP levels were increased after naloxone administration to morphine-treated rats. Propranolol did not block the hyperactivity of catecholaminergic neurons or the enhancement of cAMP observed in the heart during withdrawal. The present results indicate that heart catecholaminergic neurons play a significant role in the alterations in heart functions during morphine abstinence syndrome and suggest that those alterations are mediated through cAMP.

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Further characterization of [3H]U69593 binding sites in the rat heart

Cited by 25 publications

References 19 publications

Upregulation of the kappa opioidergic system in left ventricular rat myocardium in response to volume overload

Upregulation of the kappa opioidergic system in left ventricular rat myocardium in response to volume overload

Opioid-induced Cardioprotection

Catecholaminergic activity and 3',5'-cyclic adenosine monophosphate levels in heart right ventricle after naloxone induced withdrawal

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