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J Appl Physiol (May 17, 2002). doi:10.1152/japplphysiol.00237.2002
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Articles in PresS, published online ahead of print May 17, 2002
J Appl Physiol, 10.1152/jap.00237.2002
Submitted on March 19, 2002
Accepted on May 13, 2002

{alpha},ß Methylene ATP Elicits a Reflex Pressor Response Arising from Muscle in Decerebrate Cats

Ramy L Hanna1*, Shawn G Hayes1, and Marc P Kaufman1

1 Department of Internal Medicine, UC Davis, Davis, CA, USA

* To whom correspondence should be addressed. E-mail: rlhanna{at}ucdavis.edu.

In part the exercise pressor reflex is believed to be evoked by chemical stimuli signaling that blood supply to exercising muscles is not adequate to meet its metabolic demands. There is evidence that either adenosine 3', 5'- triphosphate (ATP) or adenosine may function as one of these chemical stimuli. For example, muscle interstitial concentrations of both substances have been found to increase during exercise. This finding led us to test the hypothesis that popliteal arterial injection of {alpha}, ß methylene ATP (5, 20, and 50 ug/ kg), which stimulates P2X receptors, and 2-chloroadenosine (25ug/ kg), which stimulates P1 receptors, evoke reflex pressor responses in decerebrate unanesthetized cats. We found that popliteal arterial injection of the two highest doses of {alpha}, ßmethylene ATP evoked pressor responses, whereas popliteal arterial injection of 2-chloroadenosine did not. In addition, the pressor responses evoked by {alpha}, ß methylene ATP were blocked either by section of the sciatic nerve or by prior popliteal arterial injection of PPADS (10 mg/kg), a selective P2 receptor antagonist. We conclude that the stimulation of P2 receptors, which are accessible through the vascular supply of skeletal muscle, evokes reflex pressor responses. In addition, our findings are consistent with the hypothesis that the stimulation of P2 receptors comprise part of the metabolic error signal evoking the exercise pressor reflex.




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