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1 Divison of Cardiology, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey, PA, USA
2 Divison of Cardiology, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey, PA, USA; Lebanon VA Medical Center, Lebanon, PA, USA
* To whom correspondence should be addressed. E-mail: jzl10{at}psu.edu.
Previous studies have suggested that activation of ATP sensitive-P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex. In order to determine the role ATP plays in this reflex it is necessary to examine if muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in twelve decerebrate cats. Interstitial muscle ATP was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 Hz and 5 Hz increased mean arterial pressure (MAP) 13±2 mmHg and 16±3 mmHg (P < 0.05), respectively; and increased ATP concentration in contracting muscle 150% (P < 0.05) and 200% (P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5 Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.
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