Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články, přehledy
PubMed
27643938
DOI
10.33549/physiolres.933391
PII: 933391
Knihovny.cz E-zdroje
- MeSH
- antiarytmika farmakologie terapeutické užití MeSH
- antioxidancia farmakologie terapeutické užití MeSH
- hypertenze farmakoterapie metabolismus patologie MeSH
- konexin 43 metabolismus MeSH
- lidé MeSH
- melatonin farmakologie terapeutické užití MeSH
- mezerový spoj ultrastruktura MeSH
- myokard ultrastruktura MeSH
- oleje rostlin farmakologie terapeutické užití MeSH
- omega-3 mastné kyseliny farmakologie terapeutické užití MeSH
- srdce účinky léků MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- antiarytmika MeSH
- antioxidancia MeSH
- GJA1 protein, human MeSH Prohlížeč
- konexin 43 MeSH
- melatonin MeSH
- oleje rostlin MeSH
- omega-3 mastné kyseliny MeSH
Gap junction connexin channels are important determinants of myocardial conduction and synchronization that is crucial for coordinated heart function. One of the main risk factors for cardiovascular events that results in heart attack, congestive heart failure, stroke as well as sudden arrhythmic death is hypertension. Mislocalization and/or dysfunction of specific connexin-43 channels due to hypertension-induced myocardial remodeling have been implicated in the occurrence of life-threatening arrhythmias and heart failure in both, humans as well as experimental animals. Recent studies suggest that down-regulation of myocardial connexin-43, its abnormal distribution and/or phosphorylation might be implicated in this process. On the other hand, treatment of hypertensive animals with cardioprotective drugs (e.g. statins) or supplementation with non-pharmacological compounds, such as melatonin, omega-3 fatty acids and red palm oil protects from lethal arrhythmias. The antiarrhythmic effects are attributed to the attenuation of myocardial connexin-43 abnormalities associated with preservation of myocardial architecture and improvement of cardiac conduction. Findings uncover novel mechanisms of cardioprotective (antihypertensive and antiarrhythmic) effects of compounds that are used in clinical settings. Well-designed trials are needed to explore the antiarrhythmic potential of these compounds in patients suffering from hypertension.
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