Effects of acute hyperglycemia on the exercise pressor reflex in healthy rats

The exercise pressor reflex is exaggerated in type 2 diabetes mellitus (T2DM). Hyperglycemia, a main characteristic of T2DM, likely contributes to this exaggerated response. However, the isolated effect of acute hyperglycemia, independent of T2DM, on the exercise pressor reflex is not known. Therefore, the purpose of this study was to determine the effect of acute, local exposure to hyperglycemia on the exercise pressor reflex and its two components, namely the mechanoreflex and the metaboreflex, in healthy rats. To accomplish this, we determined the effect of an acute locol intra-arterial glucose infusion (0.25 g/mL) on cardiovascular responses to static contraction (i.e., exercise pressor reflex) and tendon stretch (i.e., mechanoreflex) for 30 s, as well as hindlimb intra-arterial lactic acid (24 mM) injection (i.e., metaboreflex) in fasted unanesthetized, decerebrated SpragueDawley rats. We measured and compared changes in mean arterial pressure (MAP) and heart rate (HR) before and after glucose infusion. We found that acute glucose infusion did not affect the pressor response to static contraction (Delta MAP: before: 15 +/- 2 mmHg, after: 12 +/- 2 mmHg; n = 8, p > 0.05), tendon stretch (Delta MAP: before: 12 +/- 1 mmHg, after: 12 +/- 3 mmHg; n = 8, p > 0.05), or lactic acid injection (Delta MAP: before: 13 +/- 2 mmHg, after: 17 +/- 3 mmHg; n = 9, p > 0.05). Likewise, cardioaccelerator responses were unaffected by glucose infusion, p > 0.05 for all. In conclusion, these findings suggest that acute, local exposure to hyperglycemia does not affect the exercise pressor reflex or either of its components.