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This Article Full Text Full Text (PDF) All Versions of this Article: 295/3/H1017    most recent 00450.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by McCord, J. L. Articles by Kaufman, M. P. PubMed PubMed Citation Articles by McCord, J. L. Articles by Kaufman, M. P.

Acid-sensing ion and epithelial sodium channels do not contribute to the mechanoreceptor component of the exercise pressor reflex

Penn State Heart and Vascular Institute, Pennsylvania State University College of Medicine, Hershey, Pennsylvania

Submitted 29 April 2008 ; accepted in final form 1 July 2008

Amiloride, injected into the popliteal artery, has been reported to attenuate the reflex pressor response to static contraction of the triceps surae muscles. Both mechanical and metabolic stimuli arising in contracting skeletal muscle are believed to evoke this effect, which has been named the exercise pressor reflex. Amiloride blocks both acid-sensing ion channels, as well as epithelial sodium channels. Nevertheless, amiloride is thought to block the metabolic stimulus to the reflex, because this agent has been shown to attenuate the reflex pressor response to injection of lactic acid into the arterial supply of skeletal muscle. The possibility exists, however, that amiloride may also block mechanical stimuli evoking the exercise pressor reflex. The mechanical component of the reflex can be assessed by measuring renal sympathetic nerve activity during the first 2–5 s of contraction. During this period of time, the sudden tension developed by contraction onset briskly discharges mechanoreceptors, whereas it has little effect on the discharge of metaboreceptors. We, therefore, examined the effect of amiloride (0.5 µg/kg) injected into the popliteal artery on the renal sympathetic and pressor responses to static contraction of the triceps surae muscles in decerebrated cats. We found that amiloride significantly attenuated the pressor and renal sympathetic responses to contraction; for the latter variable, the attenuation started 10 s after the onset of contraction. Our findings lead us to conclude that acid-sensing ion channels and epithelial sodium channels play little, if any, role in evoking the mechanical component of the exercise pressor reflex.

group III and IV muscle afferents; renal sympathetic nerves; neural control of the circulation; cats; autonomic nervous system

This article has been cited by other articles:

				S. G. Hayes, J. L. McCord, J. Rainier, Z. Liu, and M. P. Kaufman Role played by acid-sensitive ion channels in evoking the exercise pressor reflex Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1720 - H1725. [Abstract] [Full Text] [PDF]