Mechanisms mediating the muscle metaboreflex pressor response during post‐exercise muscle ischemia are altered in hypertension (1170.2)

During dynamic exercise, muscle metaboreflex activation (MMA; induced via partial hindlimb ischemia) markedly increases mean arterial pressure (MAP) and MAP is sustained when the ischemia is maintained following the cessation of exercise (post‐exercise muscle ischemia ‐ PEMI). We previously reported that the sustained pressor response during PEMI in normal individuals is driven by a sustained increase in cardiac output (CO) with no peripheral vasoconstriction. However, we have recently shown that the rise in CO with MMA is significantly blunted in hypertension (HTN). The mechanisms sustaining the pressor response during PEMI in HTN are unknown. In six chronically instrumented canines, hemodynamic responses were observed during rest, mild exercise (3.2 kph), MMA and PEMI in the same animals before and after the induction of HTN (2K1C). In control, MAP, CO and HR increased with MMA (+52 ± 6 mmHg, +2.1 ± 0.3 l/min and +37 ± 7 bpm). After the induction of HTN (MAP at rest increased from 97 ± 3 to 130 ± 4 mmHg), these responses were markedly attenuated (+32 ± 5 mmHg, +0.6 ± 0.2 l/min and +11 ± 3 bpm), yet MAP was similarly sustained during PEMI while CO and peripheral vascular conductance were significantly lower (5.2 ± 0.2 l/min and 32 ± 3 ml/min/mmHg vs. 4.1 ± 0.4 l/min and 26 ± 2 ml/min/mmHg). We conclude that peripheral vasoconstriction significantly contributes to the sustained pressor response during PEMI in HTN. Grant Funding Source : HL‐55743 and HL‐095819