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A murine model of the exercise pressor reflex
1Lillehei Heart Institute, University of Minnesota, Minneapolis, MN, 55455, USA.
The Journal of Physiology
|May 15, 2020
Summary
A new decerebrate mouse model allows scientists to study the exercise pressor reflex (EPR). This model helps define the mechanisms of EPR in health and disease, particularly the role of TRPV1 receptors.
Area of Science:
- Cardiovascular Physiology
- Neuroscience
- Exercise Science
Background:
- The exercise pressor reflex (EPR) increases blood pressure and heart rate during exercise.
- Mechanistic studies of EPR are difficult in humans.
- A decerebrate rodent model is needed for detailed EPR research.
Purpose of the Study:
- To develop and validate a decerebrate mouse model for studying the EPR.
- To investigate the role of TRPV1 receptors in mediating the EPR.
- To enable future research on EPR mechanisms in various mouse models.
Main Methods:
- Developed a decerebrate mouse model.
- Used ventral root stimulation (VRS) to elicit cardiovascular responses.
- Administered TRPV1 antagonists and used Trpv1 null mice.
- Performed dorsal rhizotomy and neuromuscular blockade.
Main Results:
- Decerebrate mouse model mimics EPR with increased MAP and HR.
- VRS response was abolished by dorsal rhizotomy or neuromuscular blockade.
- TRPV1 antagonism or Trpv1 null mice significantly reduced MAP response to VRS and capsaicin.
Conclusions:
- The decerebrate mouse is a valid model for EPR research.
- TRPV1 receptors play a significant role in mediating the EPR.
- This model facilitates the study of cardiovascular responses to exercise in health and disease.
