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Related Experiment Videos

Gadolinium attenuates exercise pressor reflex in cats.

S G Hayes1, M P Kaufman

  • 1Division of Cardiovascular Medicine, Departments of Internal Medicine and Human Physiology, University of California, Davis, California 95616, USA. sghayes@ucdavis.edu

American Journal of Physiology. Heart and Circulatory Physiology
|April 12, 2001
PubMed
Summary

Mechanical stimuli, not just metabolic signals, contribute to the exercise pressor reflex. Gadolinium blocked these mechanical responses, suggesting a role for mechanosensitive channels in muscle afferents during exercise.

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Area of Science:

  • Cardiovascular Physiology
  • Skeletal Muscle Physiology
  • Neuroscience

Background:

  • The exercise pressor reflex (EPR) increases blood pressure during physical activity.
  • It's traditionally attributed to metabolic stimuli from working muscles.
  • The role of mechanical stimuli in EPR is less understood.

Purpose of the Study:

  • To investigate the contribution of mechanical stimuli to the EPR.
  • To determine if mechanosensitive channels are involved in EPR.

Main Methods:

  • Used decerebrate and anesthetized cats.
  • Administered gadolinium, a mechanosensitive channel blocker, via femoral artery injection.
  • Measured reflex pressor responses to static muscle contraction and tendon stretch.

Related Experiment Videos

  • Recorded afferent nerve activity from group III and IV muscle afferents.

    • Main Results:

    • Gadolinium significantly attenuated pressor responses to muscle contraction and tendon stretch.
    • Gadolinium did not affect pressor responses to capsaicin (a metabolic stimulus).
    • Gadolinium reduced activity in mechanically sensitive group III afferents but not metabolically sensitive group IV afferents.

    Conclusions:

    • Mechanical stimuli play a significant role in evoking the exercise pressor reflex.
    • Mechanosensitive channels in muscle afferents contribute to the EPR.
    • Findings challenge the purely metabolic view of EPR initiation.