U50,488H Inhibits Effects of Norepinephrine in Rat Cardiomyocytes—Cross-Talk between κ-opioid and β-adrenergic Receptors

Yu, Xiao Chun; Li, Hong Yu; Wang, Hong Xin; Wong, Tak Ming

doi:10.1006/jmcc.1997.0604

Cited by 42 publications

(8 citation statements)

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“…Chemical sympathectomy reduces the amount of dynorphin in the heart, indicating that κ-opioid peptides may co-exist with the catecholamines in the sympathetic nerve terminal (Wegener and Kummer, 1994; Pepe et al, 2004). The activation of κ-OR with a selective exogenous agonist U50, 488H inhibits the effects of β-adrenergic receptor (β-AR) agonist to increase rat myocyte contractility (Yu et al, 1998). These inhibitory effects are antagonized by a selective κ-OR antagonist, indicating that the effects are κ-OR mediated (Yu et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…The activation of κ-OR with a selective exogenous agonist U50, 488H inhibits the effects of β-adrenergic receptor (β-AR) agonist to increase rat myocyte contractility (Yu et al, 1998). These inhibitory effects are antagonized by a selective κ-OR antagonist, indicating that the effects are κ-OR mediated (Yu et al, 1998). A disturbed cross-talk between κ-OR and β-AR (Pepe et al, 2004) by significant reduction in or absence of the inhibition of β-AR stimulation by κ-OR stimulation may lead to an excessive increase in cardiac activity leading to disproportionately increased BP (Wong and Shan, 2001).…”

Section: Discussionmentioning

confidence: 99%

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Effects of perinatal oxycodone exposure on the cardiovascular response to acute stress in male rats at weaning and in young adulthood

Sithisarn¹,

Bada²,

Charnigo³

et al. 2013

Front. Physiol.

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Oxycodone (OXY) is one of the most commonly abused opiates during pregnancy. Perinatal opiate exposure (POE) is associated with neurobehavioral and hormone changes. Little is known about the effects of perinatal OXY on the cardiovascular (CV) responses to stress.Objectives: to determine the effects of POE on: (1) CV responses to acute stress and ability to discriminate using a classical conditioning paradigm; (2) changes in CV response to the paradigm and retention of the ability to discriminate from postnatal day (PD) 40 to young adulthood.Methods: Pregnant rats were given i.v. OXY or vehicle (CON) daily. OXY and CON males were fitted with BP telemetry units. Offspring were classically conditioned by following a pulsed tone (CS+) with tail shock. A steady tone (CS−) was not followed by shock. BP and HR were recorded during resting periods and conditioning. Changes in BP, HR from composite analysis were compared. The paradigm was repeated on PD 75.Results: At PD 40, OXY rats had a lower baseline mean BP (OXY: 114.8 ± 1.0 vs. CON: 118.3 ± 1.0 mm Hg; mean ± SEM) but larger amplitude of the conditional BP increase during the stress response (OXY: +3.9 ± 0.4 vs. CON: +1.7 ± 0.4 mm Hg). Both OXY and CON rats were able to discriminate between CS+ and CS−. At PD 75, the effects of OXY on the increased amplitude of the conditional BP had dissipated (CON: +3.4 ± 2.3 vs. OXY: +4.5 ± 1.4 mm Hg). BP responses to the stress and non-stress stimuli did not differ in the OXY group, suggesting that OXY may have decreased the ability of the offspring to discriminate (OXY: CS+: 147.1 ± 1.6, CS−: 145.9 ± 1.6 mm Hg vs. CON: CS+: 155.4 ± 2.7, CS−: 147.8 ± 2.7 mm Hg).Conclusion: POE is associated with subtle alterations in stress CV responses in weanling rats which dissipate when the conditioning is repeated at an early adult age. Although POE effect on the ability to discriminate at weanling age could not be detected, POE may impair retention of this ability in adulthood.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of perinatal oxycodone exposure on the cardiovascular response to acute stress in male rats at weaning and in young adulthood

Sithisarn¹,

Bada²,

Charnigo³

et al. 2013

Front. Physiol.

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“…In isolated rat hearts, a marked anti-adrenergic effect of the δ-receptor agonist leu-enkephalin, due to its postsynaptic action on the β 1 -adrenergic receptor was observed; this likely occurred via a pertussis toxin (PTX)-sensitive G-protein involved in adenylyl cyclase inhibition [45]. Likewise, cross-talk between κ-opioid and β-adrenergic receptors has been reported [46, 47]. The effects of norepinephrine on both contraction and [Ca 2+ ] i transients measured in single rat ventricular myocytes were attenuated in a dose-dependent manner by the κ-agonist U50,488H.…”

Section: The Role Of Opioid Receptors In Opioid-induced Cardioprotmentioning

confidence: 99%

“…This suggested that κ-receptor stimulation produced inhibitory actions on β-adrenergic receptor stimulation in the heart. U50,488H also inhibited the stimulatory effects of the β-adrenoceptor agonist isoprenaline on [Ca 2+ ] i transients and cAMP accumulation in ventricular myocytes, and this cross-talk was attenuated in myocytes from chronically hypoxic, but not normoxic rats [46, 47]. This action was attributed to impaired G s -protein and adenylyl cyclase responses to κ-receptor activation and to desensitization of the receptor.…”

Section: The Role Of Opioid Receptors In Opioid-induced Cardioprotmentioning

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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“…Ventricular myocytes of Sprague Dawley rats were isolated using a collagenase perfusion method [ 18 ]. The cells were loaded with fura-2/AM as a Ca 2+ indicator, and [Ca 2+ ] i transient was determined by a spectrofluorometric method as described previously [ 19 ]. Briefly, the ventricular myocytes loaded with fura-2/AM were transferred to the stage of an inverted microscope (Nikon) in a superfusion chamber at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Anti-arrhythmic effect of acupuncture pretreatment in the rats subjected to simulative global ischemia and reperfusion—involvement of intracellular Ca2+ and connexin 43

Gao

Zhao

Wang

et al. 2015

BMC Complement Altern Med

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BackgroundThe previous study showed that the cardiac arrhythmias induced by myocardial ischemia and reperfusion were attenuated by the pretreatment of acupuncture; however, the related mechanism is not understood. The present study was therefore designed to determine whether intracellular Ca2+ ([Ca2+]i) and connexin 43 (Cx43) are involved in the mediation of the anti-arrhythmic effect of electro-acupuncture (EA) pretreatment in the rats subjected to simulative global ischemia and reperfusion (SGIR).MethodsSGIR was made in the isolated heart by a low flow perfusion followed by a flow restoration. Four groups of animals are involved in the present study, including normal control group, SGIR group, EA group and EA plus 18 beta-glycyrrhetinic acid (EAG) group. For EA pretreatment, bilateral Neiguan acupoints (PC6) of the rats were stimulated for 30 min once a day in 3 consecutive days. Cx43 antagonist was given to the rats in EAG group 30 minutes before the EA pretreatment. The resting [Ca2+]i concentration, calcium oscillation, the contents of total Cx43 and non-phosphrylated Cx43 and arrhythmia score were compared among different groups.ResultsIn EA group, the arrhythmic score, the resting [Ca2+]i concentration and the number of [Ca2+]i oscillations were all significantly less than those in SGIR group (all P < 0.05), and interestingly, after EA pretreatment, the contents of nonphosphated Cx43 in the EA group were significantly lower than that in SGIR group respectively (P < 0.05). However, when the rats were treated with Cx43 antagonist prior to the EA pretreatment, the protection effects induced by EA pretreatment were reversed.ConclusionsThe results showed that EA pretreatment could produce anti-arrhythmic effect in the rats subjected to SGIR. The anti-arrhythmic effect of EA pretreatment may be due at least partially to the inhibition of SGIR-induced calcium overload and [Ca2+]i oscillations, reduction of non-phosphorylated Cx43 and the enhancement of the corresponding phosphorylated Cx43 in the cardiac cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-015-0521-y) contains supplementary material, which is available to authorized users.

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U50,488H Inhibits Effects of Norepinephrine in Rat Cardiomyocytes—Cross-Talk between κ-opioid and β-adrenergic Receptors

Cited by 42 publications

References 0 publications

Effects of perinatal oxycodone exposure on the cardiovascular response to acute stress in male rats at weaning and in young adulthood

Effects of perinatal oxycodone exposure on the cardiovascular response to acute stress in male rats at weaning and in young adulthood

Opioid-induced Cardioprotection

Anti-arrhythmic effect of acupuncture pretreatment in the rats subjected to simulative global ischemia and reperfusion—involvement of intracellular Ca2+ and connexin 43

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