Intermittent activation of bradykinin B2 receptors and mitochondrial KATP channels trigger cardiac postconditioning through redox signaling

Penna, Cláudia; Mancardi, Daniele; Rastaldo, Raffaella; Losano, G; Pagliaro, Pasquale

doi:10.1016/j.cardiores.2007.03.001

Cited by 136 publications

(185 citation statements)

References 49 publications

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“…This supports the idea that the delayed recovery of intracellular pH during initial reperfusion, is mandatory to limit infarct size in PostC mainly via prevention of mPTP opening and prevention of RIRR [8,9,17,29,30,34,55]. Both in vitro and in vivo studies demonstrated that large spectrum ROSscavengers such as N-acetyl-L-cysteine (NAC) and/or N-(2-mercaptopropionyl)-glycine (MPG) given either during the PostC maneuvers [8,51,54,63] or during AB infusion [8,9,10,13] prevented their protective effects [13,51,54,63]. Moreover, addition of alkaline buffer in early reperfusion abolishes both AB-and PostC-protection [8,9,17,29,55].…”

Section: Introductionsupporting

confidence: 63%

“…However, we have been unable to reproduce cardioprotection with ROS generator given during early reperfusion [51]. Since ROS-scavengers (NAC or MPG) abolished AB-and PostC-induced protection [8,9,51,54,63], it is likely that the type, the concentration, and/or the compartmentalization of ROS/RNS may play a pivotal role in triggering protection at early reperfusion time.…”

Section: Introductionmentioning

confidence: 86%

“…Also PostC-protection requires ROS signaling and delayed recovery of intracellular pH during initial reperfusion. The mechanisms by which PostC alters the pathophysiology of reperfusion injury involves molecular and physiological mechanisms, such as delaying realkalinization of tissue pH [8,9,17,29,30,55], triggering release of ROS and autacoids [13,46,[50][51][52]54,61], and activation of kinases that impact cellular and subcellular targets or effectors, such as mPTP [e.g., 20, 46,50,52]. Importantly acidic buffer (AB) given for the first few minutes of reperfusion is as protective as a PostC protocol [8,9,13,17,29,30,34,55].…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, it is likely that interplays between redox and acid/base conditions in early reperfusion exist. Clearly the PostC cycles (i.e., intermittent re-oxygenation) and the early acidosis may be responsible of modifications of enzyme activities and chemical reactions, which lead to produce a few ROS with signaling role instead of ROS stress [13,51,53].…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, persistence of acidosis is important for non-enzymatic NO • production [59,69]. So that ROS in concert with NO • and reactive nitrogen species (RNS) may put the heart into a protected state [26,38,46,[49][50][51][52]63].…”

Section: Introductionmentioning

confidence: 99%

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Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Penna

Perrelli

Tullio

et al. 2011

Pflugers Arch - Eur J Physiol

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Postconditioning (PostC) modifies early post-ischemic pH, redox-environment and activity of enzymes. We hypothesized that early acidosis in PostC may affect superoxide-dismutase (SOD) and catalase(CAT) activities, may reduce 3-nitrotyrosine(3-NT)-and may increase S-nitrosylated (SNO)-protein levels, thus deploying its protective effects. To verify this hypothesis, we studied early (7 th min) and late (120 th min) phases of reperfusion a) endogenous-SOD and -CAT activities, and b) 3-NT-and SNO-protein levels. Isolated rat hearts underwent 30-min ischemia/120-min reperfusion(I/R) or PostC (5 cycles of 10-s I/R at the beginning of 120-min reperfusion) either with or without exogenous-CAT or -SOD infused during the initial 3-min of reperfusion. The effects of early reperfusion with acidic-buffer(AB, pH 6.8) on endogenous antioxidant-enzymes were also tested. Pressure, infarct-size and lactate-dehydrogenase release were also measured. At the 7 th min, PostC induced a significant decrease in SOD-activity with no major change in both Mn-and Cu/Zn-SOD levels, and in CAT-activity and level. PostC also reduced 3-NT and increased SNO levels. Exogenous-SOD, but not -CAT abolished PostCcardioprotection. In late reperfusion(120-min), I/R increased SOD-activity, but decreased CATactivity and Cu/Zn-SOD levels; these effects were reversed by PostC; 3-NT was not affected, but SNO was increased by PostC. AB reproduced PostC effects on antioxidant-enzymes.Conclusions: PostC downregulates endogenous-SOD and preserves -CAT activity, thus increasing SNO and reducing 3-NT levels. These effects are triggered by early post-ischemic acidosis. Yet acidosis-induced SOD-downregulation may limit denitrosylation; thus contributing to PostC-triggering. Hence, exogenous-SOD, but not -CAT, interferes with PostC-triggering.Persistent SOD-downregulation and SNO-increase may contribute to PostC and AB beneficial effects.

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Section: Introductionsupporting

confidence: 63%

Section: Introductionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Penna

Perrelli

Tullio

et al. 2011

Pflugers Arch - Eur J Physiol

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Treatment of Myocardial Ischemia/Reperfusion Injury by Ischemic and Pharmacological Postconditioning

Heusch

2015

Comprehensive Physiology

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Timely reperfusion is the only way to salvage ischemic myocardium from impending infarction. However, reperfusion also adds a further component to myocardial injury such that the ultimate infarct size is the result of both ischemia- and reperfusion-induced injury. Modification of reperfusion can attenuate reperfusion injury and thus reduce infarct size. Ischemic postconditioning is a maneuver of repeated brief interruption of reperfusion by short-lasting coronary occlusions which results in reduced infarct size. Cardioprotection by ischemic postconditioning is mediated through delayed reversal of acidosis and the activation of a complex signal transduction cascade, including triggers such as adenosine, bradykinin, and opioids, mediators such as protein kinases and, notably, mitochondrial function as effector. Inhibition of the mitochondrial permeability transition pore appears to be a final signaling step of ischemic postconditioning. Several drugs which recruit in part such signaling steps of ischemic postconditioning can induce cardioprotection, even when the drug is only administered at reperfusion, that is, there is also pharmacological postconditioning. Ischemic and pharmacological postconditioning have been translated to patients with acute myocardial infarction in proof-of-concept studies, but further mechanistic insight is needed to optimize the conditions and algorithms of cardioprotection by postconditioning.

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Synergistic effect of low‐frequency ultrasound and low‐dose bradykinin on increasing permeability of the blood–tumor barrier by opening tight junction

Zhang

Chun-yi

Xue

et al. 2009

J of Neuroscience Research

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Low-frequency ultrasound (LFU) and bradykinin (BK) have been shown separately to increase the permeability of the blood-tumor barrier (BTB) in the rat model of C6 glioma. This study examined the hypothesis that the combination of LFU and low-dose BK has a synergistic effect on increasing the permeability of BTB and explored the possible underlying mechanism including the involvement of tight junction (TJ). The rats were divided into six groups: control group, LFU group, BK group, 2/3LFU + 1/2BK group, 5/6LFU + 2/3BK group, and LFU + BK group. The BTB permeability was assessed by Evans blue extravasation. The mRNA and protein expressions of TJ-related proteins ZO-1, occludin, and claudin-5 were determined by reverse transcriptase-polymerase chain reaction, immunohistochemistry, immunolocalization, and Western blot test. BTB permeability increased in all the experimental groups, accompanied by opening of local TJ of the BTB, observed by transmission electron microscopy, and decreased mRNA and protein expressions of ZO-1, occludin, and claudin-5. In addition, there was a further increase in BTB permeability and a further reduction in the expressions of TJ-related proteins in 5/6LFU + 2/3BK and LFU + BK groups, compared with LFU or BK group. These results indicate that LFU and low-dose BK applied in combination act in a synergistic manner to increase BTB permeability. The down-regulation of TJ-related proteins ZO-1, occludin, and claudin-5 may be one of the underlying mechanisms of the increase in BTB permeability induced by LFU and BK.

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Intermittent activation of bradykinin B2 receptors and mitochondrial KATP channels trigger cardiac postconditioning through redox signaling

Cited by 136 publications

References 49 publications

Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Treatment of Myocardial Ischemia/Reperfusion Injury by Ischemic and Pharmacological Postconditioning

Synergistic effect of low‐frequency ultrasound and low‐dose bradykinin on increasing permeability of the blood–tumor barrier by opening tight junction

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