Protection against infarction afforded by preconditioning is mediated by A1 adenosine receptors in rabbit heart.

Liu, G. S.; Thornton, J D; Winkle, Donna M. Van; Stanley, Alfred W.H.; Olsson, R A; Downey, James M.

doi:10.1161/01.cir.84.1.350

Cited by 1,255 publications

(570 citation statements)

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“…Indeed, it has been proposed that the cardioprotective effects of ischaemic preconditioning are secondary to the release of endogenous mediators such as adenosine (Liu et al, 1991;Thornton et al, 1992) which, via the stimulation of G protein-coupled (Gq/Go) receptors and activation of PKC, ultimately leads to the long-lasting opening of KATP channels. Similarly, the reductions in infarct size caused by E-type prostaglandins, such as PGEI, and by endothelin-l are due to the activation of KATP channels, as the cardioprotective effects of these autacoids are attenuated by glibenclamide and 5-HD (Hide et al, 1995a,b).…”

Section: Discussionmentioning

confidence: 99%

Sulprostone‐induced reduction of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Hide

Thiemermann

1996

British J Pharmacology

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1 This study examined whether (i) a 1 h pretreatment with or (ii) a continuous infusion of sulprostone reduces myocardial infarct size arising from coronary artery occlusion (60 min) and reperfusion (120 min) in the anaesthetized rabbit. In addition, we investigated whether the observed cardioprotective effect of this selective agonist of prostanoid EP,/EP3 receptors were due to the activation of ATPsensitive potassium (KATP) channels.2 In anaesthetized rabbits pretreated with vehicle (5% ethanol in 0.9% saline; 0.05 ml min-', i.v.) infarct size (expressed as a percentage of the area at risk) after 60 min of coronary artery occlusion followed by 120 min of reperfusion was 59 + 4% (n = 10). Pretreatment of rabbits with sulprostone (1.0 ug kg-' min-' for 1 h, discontinued immediately prior to coronary artery occlusion) did not reduce infarct size (60 + 4%; n = 4). In contrast, a continuous infusion of sulprostone (1.0 ig kg-' min-') starting 10 min prior to the onset of LAL occlusion and continued throughout the experiment, significantly reduced infarct size (41 + 5%, n = 6) when compared to the respective vehicle-treated controls (57 + 4%, n = 10; P <0.05). Sulprostone (pretreatment or continuous infusion) had no effect on any of the haemodynamic parameters measured. 3 The reduction in infarct size afforded by continuous infusion of sulprostone was abolished by pretreatment of rabbits with the KATP channel blocker 5-hydroxydecanoate (5-HD 5 pg kg-'; 63+4%; n =6). When administered alone, 5-HD had no effect on infarct size when compared to control (52+6, n=10). 4 We propose that a continuous infusion of the selective EP,/EP3 prostanoid receptor agonist, sulprostone, reduces infarct size in the anaesthetized rabbit by a mechanism that involves the opening of KATP channels.

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Section: Discussionmentioning

confidence: 99%

Sulprostone‐induced reduction of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Hide

Thiemermann

1996

British J Pharmacology

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“…Experimentally, it is the most powerful form of cardiac protection known and it has been demonstrated in cardiac myocytes [2][3][4][5], intact hearts [6,7] and many animal species [8][9][10][11], including humans [12][13][14]. Downstream signalling molecules reported to be involved in PC include ATPdependent potassium channels [4,12,15,16], PKC (protein kinase C) isoenzymes [2, 3,12,15,17,18], MAPK (mitogen-activated protein kinase) enzymes [19][20][21], tyrosine kinases [22][23][24], PI3K (phosphoinositide 3-kinase) [22,25], heat-shock proteins [5,16,26], nitric oxide [27][28][29], free radicals [21,25,30] etc.…”

Section: Introductionmentioning

confidence: 99%

Protein kinase Cϵ interacts with cytochrome c oxidase subunit IV and enhances cytochrome c oxidase activity in neonatal cardiac myocyte preconditioning

Ogbi

Johnson

2005

Biochemical Journal

117

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We have previously identified a phorbol ester-induced PKCϵ (protein kinase Cϵ) interaction with the (∼18 kDa) COIV [CO (cytochrome c oxidase) subunit IV] in NCMs (neonatal cardiac myocytes). Since PKCϵ has been implicated as a key mediator of cardiac PC (preconditioning), we examined whether hypoxic PC could induce PKCϵ–COIV interactions. Similar to our recent study with phorbol esters [Ogbi, Chew, Pohl, Stuchlik, Ogbi and Johnson (2004) Biochem. J. 382, 923–932], we observed a time-dependent increase in the in vitro phosphorylation of an approx. 18 kDa protein in particulate cell fractions isolated from NCMs subjected to 1–60 min of hypoxia. Introduction of a PKCϵ-selective translocation inhibitor into cells attenuated this in vitro phosphorylation. Furthermore, when mitochondria isolated from NCMs exposed to 30 min of hypoxia were subjected to immunoprecipitation analyses using PKCϵ-selective antisera, we observed an 11.1-fold increase in PKCϵ–COIV co-precipitation. In addition, we observed up to 4-fold increases in CO activity after brief NCM hypoxia exposures that were also attenuated by introducing a PKCϵ-selective translocation inhibitor into the cells. Finally, in Western-blot analyses, we observed a >2-fold PC-induced protection of COIV levels after 9 h index hypoxia. Our studies suggest that a PKCϵ–COIV interaction and an enhancement of CO activity occur in NCM hypoxic PC. We therefore propose novel mechanisms of PKCϵ-mediated PC involving enhanced energetics, decreased mitochondrial reactive oxygen species production and the preservation of COIV levels.

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“…It has been demonstrated that Gi protein-coupled receptors mediate the cardioprotection of IPC (Liu et al, 1991;Schultz et al, 1998). The kappa opioid receptor (k-OR) is one of the receptors that mediate the cardioprotection of IPC (Wang et al, 2001a) and the action of its stimulation is mediated via a pertussis toxin-sensitive G-protein (Sheng et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

The K_Ca channel as a trigger for the cardioprotection induced by kappa‐opioid receptor stimulation – its relationship with protein kinase C

Cao

Chen

Wong

2005

British J Pharmacology

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1 We first determined whether the cardioprotection resulting from kappa opioid receptor (k-OR) stimulation was blocked by the K Ca channel inhibitor, paxilline (Pax), administered before or during ischaemic insults in vitro. 2 In isolated rat hearts, 30 min of ischaemia and 120 min of reperfusion induced infarction and increased lactate dehydrogenase (LDH) release. In isolated ventricular myocytes subjected to 5 min of metabolic inhibition and anoxia followed by 10 min of reperfusion, the percentage of live cells and the amplitude of the electrically induced intracellular Ca 2 þ ([Ca 2 þ ] i ) transient decreased, while diastolic [Ca 2 þ ] i increased. Pretreatment with 10 mM U50,488H, a k-OR agonist, attenuated the undesirable effects of ischaemic insults in both preparations. The beneficial effects of k-OR stimulation, that were abolished by 5 mM nor-BNI, a k-OR antagonist, were also abolished by 1 mM Pax administered before ischaemic insults or 20 mM atractyloside, an opener of the mitochondrial permeability transition pore. 3 Activation of protein kinase C (PKC) with 0.1 mM phorbol 12-myristate 13-acetate decreased the infarct size and LDH release in isolated rat hearts subjected to ischaemia/reperfusion, and these effects were abolished by blockade of PKC with its inhibitors, 10 mM GF109203X or 5 mM chelerythrine, and more importantly by 1 mM Pax. On the other hand, the cardioprotective effects of opening the K Ca channel with 10 mM NS1619 were not altered by either PKC inhibitor. 4 In conclusion, the high-conductance K Ca channel triggers cardioprotection induced by k-OR stimulation that involves inhibition of MPTP opening. The K Ca channel is located downstream of PKC.

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Protection against infarction afforded by preconditioning is mediated by A1 adenosine receptors in rabbit heart.

Abstract: We conclude that adenosine released during the preconditioning occlusion stimulates cardiac A1 receptors, which leaves the heart protected against infarction even after the adenosine has been withdrawn.

Cited by 1,255 publications

References 20 publications

Sulprostone‐induced reduction of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Sulprostone‐induced reduction of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Protein kinase Cϵ interacts with cytochrome c oxidase subunit IV and enhances cytochrome c oxidase activity in neonatal cardiac myocyte preconditioning

The K_Ca channel as a trigger for the cardioprotection induced by kappa‐opioid receptor stimulation – its relationship with protein kinase C

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Protection against infarction afforded by preconditioning is mediated by A1 adenosine receptors in rabbit heart.

Abstract: We conclude that adenosine released during the preconditioning occlusion stimulates cardiac A1 receptors, which leaves the heart protected against infarction even after the adenosine has been withdrawn.

Cited by 1,255 publications

References 20 publications

Sulprostone‐induced reduction of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Sulprostone‐induced reduction of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Protein kinase Cϵ interacts with cytochrome c oxidase subunit IV and enhances cytochrome c oxidase activity in neonatal cardiac myocyte preconditioning

The KCa channel as a trigger for the cardioprotection induced by kappa‐opioid receptor stimulation – its relationship with protein kinase C

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The K_Ca channel as a trigger for the cardioprotection induced by kappa‐opioid receptor stimulation – its relationship with protein kinase C