HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 581/3/1271    most recent jphysiol.2007.129197v1 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 Citing Articles via Google Scholar Google Scholar Articles by Hayes, S. G. Articles by Kaufman, M. P. Search for Related Content PubMed PubMed Citation Articles by Hayes, S. G. Articles by Kaufman, M. P. Related Collections Skeletal Muscle and Exercise

¹ Division of Cardiovascular Medicine, University of California, Davis, CA 95616, USA

Although thin fibre muscle afferents possess acid sensing ion channels (ASICs), their contribution to the exercise pressor reflex is not known. This lack of information is partly attributable to the fact that there is no known selective in vivo antagonist for ASICs. Although amiloride has been shown to antagonize ASICs, it also has been shown to antagonize voltage-gated sodium channels, thereby impairing impulse conduction in sensory nerves. Our aim was to test the hypothesis that lactic acid accumulation in exercising muscle acted on ASICs located on thin fibre muscle afferents to evoke the metabolic component of the exercise pressor reflex. To test this hypothesis, we determined in decerebrate cats if amiloride attenuated the pressor and cardioaccelerator responses to static contraction, to tendon stretch and to arterial injections of lactic acid and capsaicin. We found a dose of amiloride (0.5 µg kg^–1; I.A.) that attenuated the pressor and cardioaccelerator responses to both contraction and lactic acid injection, but had no effect on the responses to stretch and capsaicin. A higher dose of amiloride (5 µg kg^–1, I.A.) not only blocked the pressor and cardioaccelerator responses to lactic acid and contraction, but also attenuated the responses to stretch and to capsaicin, manoeuvers in which ASICs probably play no significant role. In addition, we found that the low dose of amiloride (0.5 µg kg^–1) had no effect on the responses of muscle spindles to tendon stretch and to succinylcholine, whereas the high dose (5 µg kg^–1) attenuated the responses to both. Our data suggest the low dose of amiloride used in our experiments selectively blocked ASICs, whereas the high dose blocked ASICs and impulse conduction in muscle afferents. We conclude that ASICs play a role in the metabolic component of the exercise pressor reflex.

(Received 25 January 2007; accepted after revision 26 March 2007; first published online 29 March 2007)
Corresponding author S. G. Hayes: Penn State Heart and Vascular Institute, 500 University Drive, H047, Hershey, PA 17036, USA. Email: shayes1{at}hmc.psu.edu

This article has been cited by other articles:

				Z. Gao, S. Koba, L. Sinoway, and J. Li 20-HETE increases renal sympathetic nerve activity via activation of chemically and mechanically sensitive muscle afferents J. Physiol., May 15, 2008; 586(10): 2581 - 2591. [Abstract] [Full Text] [PDF]

				H. A. Drummond, N. L. Jernigan, and S. C. Grifoni Sensing Tension: Epithelial Sodium Channel/Acid-Sensing Ion Channel Proteins in Cardiovascular Homeostasis Hypertension, May 1, 2008; 51(5): 1265 - 1271. [Full Text] [PDF]