Renal inflammation and immune cell infiltration in rats with congestive heart failure: role of renal nerves

Congestive heart failure (CHF) is a chronic condition characterized by sympathoexcitation, concurrent fluid and sodium retention. Renal inflammation, specifically in the context of chronic kidney disease (CKD), is characterized by elevated proinflammatory markers that contribute significantly to renal injury, progression to end-stage renal disease, and worsening associated cardiovascular complications, which have been commonly observed in cardiorenal disease. However, the contribution of renal nerves to renal inflammation in CHF remains to be examined. The objective of the present study was to examine the role of renal nerves in renal inflammation in rats with CHF. Coronary artery ligation was performed to induce CHF. Four weeks after surgery, bilateral renal denervation (RDN) was performed on SHAM and CHF rats. Rats were randomly divided into four groups (Sham, Sham+RDN, CHF and CHF+RDN). Flow cytometry and Western blot analysis were performed to evaluate renal inflammation (proinflammatory markers: IL-6, TNF-alpha, IL-1beta, and MCP-1) and immune cell infiltration. Rats with CHF exhibited significantly enhanced expression of proinflammatory markers (IL-6, TNF-alpha, IL1-beta and MCP-1), immune cell infiltration and activation (T-cells) compared to SHAM, indicating renal inflammation. Bilateral RDN exhibited significant reduction in proinflammatory markers, IL-6 (0.041±0.003 vs. 0.052±0.002, P< 0.05), TNF-alpha (0.029±0.003 vs. 0.043±0.003, P< 0.05), IL-1beta (0.023±0.002 vs. 0.033±0.002, P< 0.05) and MCP-1 (0.054±0.003 vs. 0.068±0.003, P< 0.05) in rats with CHF. These data indicate that increased renal nerve activity in rats with CHF contributes to enhancing the expression of proinflammatory markers, immune cell infiltration and activation, whereas RDN significantly reduced proinflammatory markers, indicating the contribution of renal nerves in renal inflammation in rats with CHF. This study was funded by NIH R01-DK-129311. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.