Abstract

Purinergic 2X (P2X) receptors on the endings of thin fiber afferents have been shown to play a role in evoking the exercise pressor reflex in cats. In this study, we attempted to extend this finding to decerebrated, unanesthetized rats whose femoral arteries were either freely perfused or were ligated 72 hours before the start of the experiment. We first established that our dose of PPADS (10 mg/ kg), a P2X receptor antagonist, attenuated the pressor response to α, β methylene ATP (10 µg/ kg), a P2X receptor agonist. We then compared the exercise pressor reflex before and after infusing PPADS into the arterial supply of the hind limb muscles that were statically contracted. In rats with freely perfused femoral arteries, the peak pressor responses to contraction were not significantly attenuated by PPADS (before PPADS: 19±2mmHg, 13 min after PPADS: 17±2mmHg, and 25 min after PPADS: 17±3mmHg). Likewise, the cardioaccelerator and renal sympathetic nerve responses were not significantly attenuated. In contrast, we found that in rats whose femoral arteries were ligated, PPADS significantly attenuated the peak pressor responses to contraction (before PPADS: 37±5mmHg, 13 min after PPADS: 27±6mmHg, 25 min after PPADS: 25±5mmHg; p<0.05). Heart rate was not significantly attenuated, but renal SNA was at certain time points over the 30s contraction period. We conclude that P2X receptors play a role in evoking the exercise pressor reflex in rats whose femoral arteries were ligated, but do not play a role in evoking the reflex in rats whose femoral arteries were freely perfused.Grant Funding Source: Supported by NIH grants HL‐096570 and AR‐059397

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