Muscle metaboreflex activation during dynamic exercise evokes epinephrine release resulting in beta(2)-mediated vasodilation

作者:Kaur Jasdeep; Spranger Marty D; Hammond Robert L; Krishnan Abhinav C; Alvarez Alberto; Augustyniak Robert A; O'Leary Donal S*
来源:American Journal of Physiology - Heart and Circulatory Physiology, 2015, 308(5): H524-H529.
DOI:10.1152/ajpheart.00648.2014

摘要

Muscle metaboreflex-induced increases in mean arterial pressure (MAP) during submaximal dynamic exercise are mediated principally by increases in cardiac output. To what extent, if any, the peripheral vasculature contributes to this rise in MAP is debatable. In several studies, we observed that in response to muscle metaboreflex activation (MMA; induced by partial hindlimb ischemia) a small but significant increase in vascular conductance occurred within the nonischemic areas (calculated as cardiac output minus hindlimb blood flow and termed nonischemic vascular conductance; NIVC). We hypothesized that these increases in NIVC may stem from a metabore-flex- induced release of epinephrine, resulting in beta(2)-mediated dilation. We measured NIVC and arterial plasma epinephrine levels in chronically instrumented dogs during rest, mild exercise (3.2 km/h), and MMA before and after beta-blockade (propranolol; 2 mg/kg), alpha(1)-blockade (prazosin; 50 mu g/kg), and alpha(1) +/- beta-blockade. Both epinephrine and NIVC increased significantly from exercise to MMA: 81.9 +/- 18.6 to 141.3 +/- 22.8 pg/ml and 33.8 +/- 1.5 to 37.6 +/- 1.6 ml.min(-1).mmHg(-1), respectively. These metaboreflex-induced increases in NIVC were abolished after beta-blockade (27.6 +/- 1.8 to 27.5 +/- 1.7 ml.min(-1).mmHg(-1)) and potentiated after alpha(1)-blockade (36.6 +/- 2.0 to 49.7 +/- 2.9 ml.min(-1).mmHg(-1)), while alpha(1) +/- beta-blockade also abolished any vasodilation (33.7 +/- 2.9 to 30.4 +/- 1.9 ml.min(-1).mmHg(-1)). We conclude that MMA during mild dynamic exercise induces epinephrine release causing beta(2)-mediated vasodilation.

  • 出版日期2015-3-1