ArticleJournal of cardiovascular pharmacology2014
Angiotensin II and ischemic preconditioning synergize to improve mitochondrial function while showing additive effects on ventricular postischemic recovery.
Article in Journal of cardiovascular pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Cardioprotection Through Mitochondrial Modulation: A Systematic Review of Pharmacological Interventions in Animal Models of I/R Injury.Cardiovascular drugs and therapy · 2026Pooled it
- Effect of Cold Adaptation on the State of Cardiovascular System and Cardiac Tolerance to Ischemia/Reperfusion Injury.Iranian biomedical journal · 2024Review
- Review
- Mitochondrial angiotensin receptors and cardioprotective pathways.American journal of physiology. Heart and circulatory physiology · 2019Review
- Critical role of angiotensin II type 2 receptors in the control of mitochondrial and cardiac function in angiotensin II-preconditioned rat hearts.Pflugers Archiv : European journal of physiology · 2018Article
- Angiotensin II-preconditioning is associated with increased PKCε/PKCδ ratio and prosurvival kinases in mitochondria.Clinical and experimental pharmacology & physiology · 2017Article
- Differential expression of microRNAs in ischemic heart disease.Drug discovery today · 2015Review
- The Role of SIRT3 in Mediating Cardioprotective Effects of RAS Inhibition on Cardiac Ischemia-Reperfusion.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2015Review
- Role of cardiac renin angiotensin system in ischemia reperfusion injury and preconditioning of heart.Indian heart journalReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies indicate that the cardioprotective effects of ischemic preconditioning (IPC) against sustained ischemia/reperfusion can be replicated by angiotensin II (Ang II). However, it is not clear whether IPC and Ang II-induced preconditioning (APC) act through similar mechanisms or synergize to enhance cardioprotection. In this study, Langendorff-perfused rat hearts were subjected to IPC, APC, or their combination (IPC/APC) followed by ischemia/reperfusion. IPC, and less potently APC, significantly increased the percent recoveries of the left ventricular developed pressure, the first derivative of developed pressure, and the rate pressure product compared with control. Furthermore, the postischemic recovery of the heart was significantly higher for IPC/APC compared with IPC or APC. The improvements in cardiac function by IPC, APC, and IPC/APC were associated with similar reductions in lactate dehydrogenase release and infarct size. However, a significant improvement in mitochondrial respiration was observed with IPC/APC. The postischemic recovery observed with APC and IPC/APC was inhibited by treatment with losartan, an Ang II type-1 receptor blocker, during the preconditioning phase but not by chelerythrine, a pan-PKC inhibitor. Both drugs, however, abolished the enhanced mitochondrial respiration by IPC/APC. Altogether, these results indicate that APC and IPC interact through mechanisms that enhance cardioprotection by affecting cardiac function and mitochondrial respiration.
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Registered trials
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