Renal denervation improves cardiac function independently of afterload and restores myocardial norepinephrine levels in a rodent heart failure model
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F24%3A00599893" target="_blank" >RIV/67985823:_____/24:00599893 - isvavai.cz</a>
Alternative codes found
RIV/00023001:_____/24:00085047 RIV/00216208:11110/24:10475334 RIV/00216208:11130/24:10475334 RIV/00064203:_____/24:10475334
Result on the web
<a href="https://doi.org/10.1038/s41440-024-01580-3" target="_blank" >https://doi.org/10.1038/s41440-024-01580-3</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1038/s41440-024-01580-3" target="_blank" >10.1038/s41440-024-01580-3</a>
Alternative languages
Result language
angličtina
Original language name
Renal denervation improves cardiac function independently of afterload and restores myocardial norepinephrine levels in a rodent heart failure model
Original language description
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.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30201 - Cardiac and Cardiovascular systems
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2024
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Hypertension Research
ISSN
0916-9636
e-ISSN
1348-4214
Volume of the periodical
47
Issue of the periodical within the volume
October
Country of publishing house
DE - GERMANY
Number of pages
13
Pages from-to
2718-2730
UT code for WoS article
001154951600002
EID of the result in the Scopus database
2-s2.0-85183701253