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Division of Cardiovascular Medicine, Departments of Internal Medicine and Human Physiology, University of California, Davis, California 95616
The
exercise pressor reflex, which arises from the contraction-induced
stimulation of group III and IV muscle afferents, is widely believed to
be evoked by metabolic stimuli signaling a mismatch between
blood/oxygen demand and supply in the working muscles. Nevertheless,
mechanical stimuli may also play a role in evoking the exercise pressor
reflex. To determine this role, we examined the effect of gadolinium,
which blocks mechanosensitive channels, on the exercise pressor reflex
in both decerebrate and 
-chloralose-anesthetized cats. We found that
gadolinium (10 mM; 1 ml) injected into the femoral artery significantly
attenuated the reflex pressor responses to static contraction of the
triceps surae muscles and to stretch of the calcaneal (Achilles)
tendon. In contrast, gadolinium had no effect on the reflex pressor
response to femoral arterial injection of capsaicin (5 µg). In
addition, gadolinium significantly attenuated the responses of group
III muscle afferents, many of which are mechanically sensitive, to both
static contraction and to tendon stretch. Gadolinium, however, had no
effect on the responses of group IV muscle afferents, many of which are
metabolically sensitive, to either static contraction or to capsaicin
injection. We conclude that mechanical stimuli arising in contracting
skeletal muscles contribute to the elicitation of the exercise pressor reflex.
group III and IV muscle afferents; contraction; tendon stretch; capsaicin; autonomic nervous system
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