Heart failure (HF) has been proposed as a potential indication of renal denervation (RDN). However, the mechanisms enabling RDN to attenuate HF are not well understood, especially the central effects of RDN. The aim of this study was to decipher the mode of operation of RDN in the treatment of HF using a canine model of right ventricular rapid pacing-induced HF. Accordingly, 24 Chinese Kunming dogs were randomly grouped to receive sham procedure (sham-operated group), bilateral RDN (RDN group), rapid pacing to induce HF (HF-control group), and bilateral RDN plus rapid pacing (RDN + HF group). Echocardiography, plasma brain natriuretic peptide (BNP), and norepinephrine (NE) concentrations of randomized dogs were measured at baseline and 4 weeks after interventions, followed by histological and molecular analyses. Twenty dogs completed the research successfully and were enrolled for data analyses. Results showed that the average optical density of renal efferent and afferent nerves were significantly lower in the RDN and RDN + HF groups than in the sham-operated group, with a significant reduction of renal NE concentration. Rapid pacing in the RDN + HF and HF-control groups, compared with the sham-operated group, induced a significant increase in left ventricular end-diastolic volume and decrease in left ventricular ejection fraction and correspondingly resulted in cardiac fibrosis and dysfunction. Cardiac fibrosis evaluated by Masson's trichrome staining and the expression of transforming growth factor-β1 (TGF-β1) were significantly higher in the HF-control group than in the sham-operated group, which were remarkably attenuated by the application of the RDN technique in the RDN + HF group. In terms of central renin-angiotensin system (RAS), the expression of angiotensin II (AngII)/angiotensin-converting enzyme (ACE)/AngII type 1 receptor (AT1R) in the hypothalamus of dogs in the HF-control group, compared with the sham-operated group, was upregulated and that of the angiotensin-(1-7) [Ang-(1-7)]/ACE2 was downregulated. Furthermore, both of them were significantly attenuated by the RDN therapy in the RDN + HF group. In conclusion, the RDN technique could damage renal nerves and suppress the cardiac remodeling procedure in canine with HF while concomitantly attenuating the overactivity of central RAS in the hypothalamus.
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http://dx.doi.org/10.3389/fphys.2019.01625 | DOI Listing |
J Clin Exp Hepatol
November 2024
Department of Surgery, Section for HPB Surgery, Aarhus University Hospital, Aarhus, Denmark.
Background/aim: Post-hepatectomy liver failure (PHLF) and hepatic steatosis are evident shortly after extensive partial hepatectomy (PH) in rodents. This study aimed to extrapolate the protein expression and biological pathways involved in recovering PHLF (rPHLF) and non-recovering PHLF (nrPHLF).
Methods: Rats were randomly assigned to 90% PH or sham surgery.
Zhongguo Zhong Yao Za Zhi
October 2024
Institute of Basic Medical Sciences of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing Key Laboratory of Chinese Materia Pharmacology, National Clinical Research Center of Traditional Chinese Medicine for Cardiovascular Diseases Beijing 100091, China Heilongjiang University of Chinese Medicine Harbin 150040, China.
To explore the regulation of vasodilatory function in rats with post-infarction heart failure by salvianolic acid B(Sal-B) based on the mechanosensitive ion channel, namely Piezo1. A post-infarction heart failure model of rats was prepared by ligation of the left anterior descending coronary artery. After successful modeling, the rats were randomly divided into the model group, Sal-B group(0.
View Article and Find Full Text PDFZhonghua Wei Zhong Bing Ji Jiu Yi Xue
November 2024
Department of Hepatobiliary Pancreatic Surgery, Quzhou City People's Hospital, Quzhou 324002, Zhejiang, China. Corresponding author: Lu Genlin, Email:
Objective: To investigate whether hydrogen sulfide (HS) protects against intestinal ischemia/reperfusion (I/R) injury in rats by regulating c-Jun N-terminal kinase/activator protein-1 (JNK/AP-1) signaling pathway.
Methods: Thirty male Wistar rats were divided into sham operated group (Sham group), I/R group, and HS donor sodium hydrosulfide (NaHS) intervention group (I/R+NaHS group), with 10 rats in each group. The I/R injury model was established by blocking the superior mesenteric artery with a non-traumatic vascular clip, with 60 minutes of ischemia followed by 120 minutes of reperfusion.
Nutrients
November 2024
Department of Physiology and Pharmacology, Karolinska Institutet, 17165 Solna, Sweden.
The prevalence of cardiovascular-kidney-metabolic (CKM) syndrome is increasing rapidly, and cardiovascular complications pose significant risks in individuals with kidney disease and metabolic dysfunction. Understanding the mechanisms of CKM disorders is crucial, as is the discovery of novel preventive treatments. This study aimed to examine the therapeutic effects of a specially formulated nitric oxide-enhancing food additive in a mouse model of CKM syndrome induced by unilateral nephrectomy (UNX) in combination with chronic Western diet (WD) feeding.
View Article and Find Full Text PDFCureus
November 2024
Department of Physiology, Showa University Graduate School of Medicine, Tokyo, JPN.
Background Knee osteoarthritis (KOA) is characterized by cartilage degradation, osteophyte formation, and synovitis. Cartilage degradation in KOA begins with the loss of aggrecan, primarily due to A Disintegrin and Metalloproteinase with Thrombospondin Motif 5 (ADAMTS5), which is produced by chondrocytes and synovial cells and a key target for therapeutic intervention. Current treatments for KOA primarily focus on pain relief, as disease-modifying osteoarthritis drugs (DMOADs) remain unavailable.
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