Does ATPγS potentiate the muscle chemoreflex response to lactic acid?

Abstract

Birdsong et al. (2010) found that acute exposure to ATP potentiated ASIC evoked currents from dorsal root ganglion cells innervating muscles of rats. This finding prompted us to determine whether the results seen in vitro would translate to an in vivo preparation. We measured the pressor and cardioaccelerator responses to injecting lactic acid (24mM; 0.4mL), an ASIC agonist, into the femoral artery of decerebrated rats with either freely perfused hindlimbs (n=6) or hindlimbs whose femoral artery was ligated (n=5). This was done both before and after injecting ATPγS (200μg/kg). In freely perfused rats, the pressor response to lactic acid after ATPγS was not different from that to lactic acid before ATPγS (15±2 vs. 14±2 mmHg; p>0.05). The cardioaccelerator response to lactic acid after ATPγS was modestly greater than that evoked by lactic acid before ATPγS (3±1 vs. −2±1 bpm; p<0.05). In ligated rats, the pressor response to lactic acid was greater after ATPγS than before, although the increase was not significant (28±6 vs. 21±4 mmHg; p=0.11). The cardioaccelerator response to lactic acid after ATPγS was not significantly different from that evoked by lactic acid before ATPγS (1±2 vs. 2±2 bpm; p>0.05). We conclude that ATPγS does not potentiate the muscle chemoreflex response to lactic acid but may do so in rats with ligated femoral arteries. Supported by NIH RO1‐HL030710 and P01 HL096570.