ArticleMolecules (Basel, Switzerland)2019
Different adaptive NO-dependent Mechanisms in Normal and Hypertensive Conditions.
Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Assessment of cognition and molecular markers for neuropsychological functions in hypertension.Journal of family medicine and primary care · 2026Article
- Modulation of Cardiac Gene Expression by anti-HMGB1 in a Model of Experimental Myocardial Infarction.Physiological research · 2025Article
- Impact of High-Fat Diet on Biochemical Changes Following Experimental Myocardial Infarction.Journal of cellular and molecular medicine · 2025Article
- Role of HMGB1 in ischemia/reperfusion injury in a rat model of myocardial infarction.Scientific reports · 2025Article
- Taxifolin Reduces Blood Pressure via Improvement of Vascular Function and Mitigating the Vascular Inflammatory Response in Spontaneously Hypertensive Rats.International journal of molecular sciences · 2023Article
- Oxidative Stress in Arterial Hypertension (HTN): The Nuclear Factor Erythroid Factor 2-Related Factor 2 (Nrf2) Pathway, Implications and Future Perspectives.Pharmaceutics · 2022Review
- Butterfly Pea Flower (Antioxidants (Basel, Switzerland) · 2021Article
- Chronic L-Name-Treatment Produces Hypertension by Different Mechanisms in Peripheral Tissues and Brain: Role of Central eNOS.Pathophysiology : the official journal of the International Society for Pathophysiology · 2020Article
- Protective Effects of Polyphenols against Ischemia/Reperfusion Injury.Molecules (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Myocardial infarction (MI) remains the leading cause of death worldwide. We aimed to investigate the effect of NO deficiency on selective biochemical parameters within discreet myocardial zones after experimentally induced MI. To induce MI, the left descending coronary artery was ligated in two groups of 16-week-old WKY rats. In one group, NO production was inhibited by L-NAME (20 mg/kg/day) administration four weeks prior to ligation. Sham operations were performed on both groups as a control. Seven days after MI, we evaluated levels of nitric oxide synthase (NOS) activity, eNOS, iNOS, NFҡB/p65 and Nrf2 in ischemic, injured and non-ischemic zones of the heart. Levels of circulating TNF-α and IL-6 were evaluated in the plasma. MI led to increased NOS activity in all investigated zones of myocardium as well as circulating levels of TNF-α and IL-6. L-NAME treatment decreased NOS activity in the heart of sham operated animals. eNOS expression was increased in the injured zone and this could be a compensatory mechanism that improves the perfusion of the myocardium and cardiac dysfunction. Conversely, iNOS expression increased in the infarcted zone and may contribute to the inflammatory process and irreversible necrotic changes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.