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: 295/5/H2043    most recent 00904.2008v1 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 Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by McCord, J. L. Articles by Kaufman, M. P. Search for Related Content PubMed PubMed Citation Articles by McCord, J. L. Articles by Kaufman, M. P.

PPADS does not block contraction-induced prostaglandin E₂ synthesis in cat skeletal muscle

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

Submitted 18 August 2008 ; accepted in final form 8 September 2008

Pyridoxal-phosphate-6-azophenyl-2'-4-disulfonate (PPADS), a purinergic 2 (P₂) receptor antagonist, has been shown to attenuate the exercise pressor reflex in cats. In vitro, however, PPADS has been shown to block the production of prostaglandins, some of which play a role in evoking the exercise pressor reflex. Thus the possibility exists that PPADS blocks the exercise pressor reflex through a reduction in prostaglandin synthesis rather than through the blockade of P₂ receptors. Using microdialysis, we collected interstitial fluid from skeletal muscle to determine prostaglandin E₂ (PGE₂) concentrations during the intermittent contraction of the triceps surae muscle before and after a popliteal arterial injection of PPADS (10 mg/kg). We found that the PGE₂ concentration increased in response to the intermittent contraction before and after the injection of PPADS (both, P < 0.05). PPADS reduced the pressor response to exercise (P < 0.05) but had no effect on the magnitude of PGE₂ production during contraction (P = 0.48). These experiments demonstrate that PPADS does not block the exercise pressor reflex through a reduction in PGE₂ synthesis. We suggest that PGE₂ and P₂ receptors play independent roles in stimulating the exercise pressor reflex.

exercise pressor reflex; groups III and IV muscle afferents; neural control of the circulation; muscle microdialysis; pyridoxal-phosphate-6-azophenyl-2'-4-disulfonate