ArticleHypertension research : official journal of the Japanese Society of Hypertension2024
Renal denervation improves cardiac function independently of afterload and restores myocardial norepinephrine levels in a rodent heart failure model.
Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Renal denervation in experimental autoimmune myocarditis: association with cardiac function and changes in calcium and MAPK/ERK signaling.Basic research in cardiology · 2026Article
- The role of ventricular remodeling in the early decompensation of cardiorenal syndrome: Insight from studies with Ren-2 transgenic hypertensive rats subjected to volume overload induced using aorto-caval fistula.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Renal denervation attenuates cardiac dysfunction in HFpEF by inhibiting the ATP-P2X7-NLRP3 inflammasome axis.Basic research in cardiology · 2025Article
- Cardiorenal Syndrome and Autonomic Overactivity.Biomedicines · 2025Review
- Alterations in renal Na,K-ATPase activity and protein expression in rat models of pressure and volume overload.Scientific reports · 2025Article
- Long-Term Electrocardiographic Changes Following Renal Denervation-Left Ventricular Mass and Arrhythmia Burden.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- Impact of sodium-glucose cotransporter-2 inhibitors on pulmonary vascular cell function and arterial remodeling.World journal of cardiology · 2025Review
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15 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
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.
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