Nerve inflammation and exaggerated blood pressure response during exercise in heart failure
Neural Inflammation and Exercise Pressor Reflex in Heart Failure
This work looks at whether inflammation in nerves that sense muscle activity causes people with chronic heart failure to have oversized blood pressure and breathing responses during exercise.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Nebraska Medical Center NIH-funded |
| Lab location | 1 site (Omaha, United States) |
| Project ID | NIH-11097354 on NIH RePORTER |
What this research studies
Researchers are using heart-attack models in rats that mimic chronic heart failure to study nerves that carry signals from muscles to the spinal cord (lumbar dorsal root ganglia) for signs of macrophage-driven inflammation. They will measure how this nerve inflammation alters mechanically sensitive and chemically sensitive reflexes that raise blood pressure and breathing during physical activity, and they will examine levels of proteins such as TRPV1 in those nerves. The team will connect these molecular and cellular changes to the exaggerated exercise pressor reflex seen in heart failure. Findings could point to biological targets to reduce dangerous sympathetic over-activation during exercise.
Who could benefit from this research
Good fit: People with chronic heart failure who experience exercise intolerance, large blood pressure increases, or shortness of breath during activity are the eventual candidates who could benefit from this research.
Not a fit: People without heart failure, or those seeking immediate clinical treatments, are unlikely to receive direct benefit from this preclinical research.
Why it matters
Potential benefit: If successful, this work could lead to new ways to reduce dangerous blood pressure and breathing spikes during exercise in people with chronic heart failure by targeting nerve inflammation.
How similar studies have performed: Prior animal studies have reported abnormal exercise reflexes and altered TRPV1 levels in heart failure, but directly linking macrophage-driven nerve inflammation to these reflex changes is a newer approach.
Where this research is happening
Omaha, United States
- University of Nebraska Medical Center — Omaha, United States (Active)
Researchers
- Principal investigator: Wang, Hanjun — University of Nebraska Medical Center
- Study coordinator: Wang, Hanjun
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.