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Renal denervation improves cardiac function independently of afterload and restores myocardial norepinephrine levels in a rodent heart failure model
M. Miklovič, O. Gawryś, Z. Honetschlägerová, P. Kala, Z. Husková, S. Kikerlová, Z. Vaňourková, Š. Jíchová, A. Kvasilová, M. Kitamoto, H. Maxová, G. Puertas-Frias, T. Mráček, D. Sedmera, V. Melenovský
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články
NLK
ProQuest Central
od 2015-01-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 2015-01-01 do Před 1 rokem
- MeSH
- krysa rodu rattus MeSH
- ledviny * inervace metabolismus MeSH
- modely nemocí na zvířatech * MeSH
- myokard * metabolismus MeSH
- noradrenalin * krev metabolismus MeSH
- potkani transgenní * MeSH
- remodelace komor fyziologie MeSH
- srdce inervace patofyziologie MeSH
- srdeční selhání * patofyziologie metabolismus MeSH
- sympatektomie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Renal nerves play a critical role in cardiorenal interactions. Renal denervation (RDN) improved survival in some experimental heart failure (HF) models. It is not known whether these favorable effects are indirect, explainable by a decrease in vascular afterload, or diminished neurohumoral response in the kidneys, or whether RDN procedure per se has direct myocardial effects in the failing heart. To elucidate mechanisms how RDN affects failing heart, we studied load-independent indexes of ventricular function, gene markers of myocardial remodeling, and cardiac sympathetic signaling in HF, induced by chronic volume overload (aorto-caval fistula, ACF) of Ren2 transgenic rats. Volume overload by ACF led to left ventricular (LV) hypertrophy and dysfunction, myocardial remodeling (upregulated Nppa, MYH 7/6 genes), increased renal and circulating norepinephrine (NE), reduced myocardial NE content, increased monoaminoxidase A (MAO-A), ROS production and decreased tyrosine hydroxylase (+) nerve staining. RDN in HF animals decreased congestion in the lungs and the liver, improved load-independent cardiac function (Ees, PRSW, Ees/Ea ratio), without affecting arterial elastance or LV pressure, reduced adverse myocardial remodeling (Myh 7/6, collagen I/III ratio), decreased myocardial MAO-A and inhibited renal neprilysin activity. RDN increased myocardial expression of acetylcholinesterase (Ache) and muscarinic receptors (Chrm2), decreased circulating and renal NE, but increased myocardial NE content, restoring so autonomic control of the heart. These changes likely explain improvements in survival after RDN in this model. The results suggest that RDN has remote, load-independent and favorable intrinsic myocardial effects in the failing heart. RDN therefore could be a useful therapeutic strategy in HF.
Department of Cardiology Institute for Clinical and Experimental Medicine IKEM Prague Czech Republic
Department of Pathophysiology 2nd Faculty of Medicine Charles University Prague Czech Republic
Institute of Anatomy 1st Faculty of Medicine Charles University Prague Czech Republic
Institute of Physiology Czech Academy of Sciences Prague Czech Republic
Citace poskytuje Crossref.org
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