|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Penn State University
* To whom correspondence should be addressed. E-mail: jmccord{at}hmc.psu.edu.
The exercise pressor reflex is evoked by both mechanical and metabolic stimuli arising in contracting skeletal muscle. Recently, blockade of acid sensing ion channels (ASICs) with amiloride and A-316567 attenuated the reflex. Moreover, amiloride had no effect on the mechanoreceptor component of the reflex, prompting us to determine if ASICs contributed to the metaboreceptor component of the exercise pressor reflex. The metaboreceptor component can be assessed by measuring mean arterial pressure during post contraction circulatory occlusion when only metaboreceptors are stimulated. We examined the effects of amiloride (0.5 µg/kg), A-317567 (10mM, 0.5 ml), and saline (0.5 ml) on the pressor response to and after static contraction while the circulation was occluded in 30 decerebrated cats. Amiloride (n=11) and A-317567 (n=7), injected into the arterial supply of the triceps surae muscles, attenuated the pressor responses both to contraction while the circulation was occluded and to post contraction circulatory occlusion (all P<0.05). Saline (n=11), however, had no effect on the pressor responses to contraction while the circulation was occluded or to post contraction circulatory occlusion (both P>0.79). Our findings lead us to conclude that ASICs contribute to the metaboreceptor component of the exercise pressor reflex.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |