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: 578/1/301    most recent jphysiol.2006.119271v1 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 Kindig, A. E. Articles by Kaufman, M. P. Search for Related Content PubMed PubMed Citation Articles by Kindig, A. E. Articles by Kaufman, M. P.

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

ATP, by activating purinergic 2 (P2) receptors on group III and IV afferents, is thought to evoke the metabolic component of the exercise pressor reflex. Previously we have shown that injection of PPADS, a P2 receptor antagonist, into the arterial supply of skeletal muscle of decerebrated cats attenuated the responses of group III and IV afferents to static contraction while the muscles were freely perfused. We have now tested the hypothesis that injection of PPADS (10 mg kg^–1) attenuated the responses of group III (n = 13) and group IV afferents (n = 9) to post-contraction circulatory occlusion. In the present study, we found that PPADS attenuated the group III afferent responses to static contraction during circulatory occlusion (P < 0.05). Likewise, PPADS abolished the group IV afferent responses to static contraction during occlusion (P = 0.001). During a 1 minute period of post-contraction circulatory occlusion, four of the 13 group III afferents and eight of the nine group IV afferents maintained their increased discharge. A Fischer's exact probability test revealed that more group IV afferents than group III afferents were stimulated by post-contraction circulatory occlusion (P < 0.02). In addition, the nine group IV afferents increased their mean discharge rate over baseline levels during the post-contraction circulatory occlusion period, whereas the 13 group III afferents did not (P < 0.05). PPADS abolished this post-contraction increase in discharge by the group IV afferents (P < 0.05). Our findings suggest that P2 receptors on group IV afferents play a role in evoking the metabolic component of the exercise pressor reflex.

(Received 15 August 2006; accepted after revision 11 October 2006; first published online 12 October 2006)
Corresponding author A. E. Kindig: TB-172, Division of Cardiovascular Medicine, University of California Davis, Davis, CA 95616, USA. Email: aekindig{at}ucdavis.edu

This article has been cited by other articles:

				J. Gonzalez-Alonso, S. P. Mortensen, T. D. Jeppesen, L. Ali, H. Barker, R. Damsgaard, N. H. Secher, E. A. Dawson, and S. P. Dufour Haemodynamic responses to exercise, ATP infusion and thigh compression in humans: insight into the role of muscle mechanisms on cardiovascular function J. Physiol., May 1, 2008; 586(9): 2405 - 2417. [Abstract] [Full Text] [PDF]

				P. G. Martin, N. Weerakkody, S. C. Gandevia, and J. L. Taylor Group III and IV muscle afferents differentially affect the motor cortex and motoneurones in humans J. Physiol., March 1, 2008; 586(5): 1277 - 1289. [Abstract] [Full Text] [PDF]

				I. Biaggioni Autonomic/metabolic interactions modulating the exercise pressor reflex: the purinergic hypothesis J. Physiol., January 1, 2007; 578(1): 5 - 6. [Full Text] [PDF]