title: Muscle metaboreflex activation during dynamic exercise evokes epinephrine release resulting in β2-mediated vasodilation.
abstract: 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 metaboreflex-induced release of epinephrine, resulting in β2-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 β-blockade (propranolol; 2 mg/kg), α1-blockade (prazosin; 50 μg/kg), and α1 + β-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 β-blockade (27.6 ± 1.8 to 27.5 ± 1.7 ml·min(-1)·mmHg(-1)) and potentiated after α1-blockade (36.6 ± 2.0 to 49.7 ± 2.9 ml·min(-1)·mmHg(-1)), while α1 + β-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 β2-mediated vasodilation.
authors.affiliation: Department of Physiology and Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan.
authors.forename: Jasdeep
authors.initials: J
authors.lastname: Kaur
authors.affiliation: Department of Physiology and Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan.
authors.forename: Marty D
authors.initials: MD
authors.lastname: Spranger
authors.affiliation: Department of Physiology and Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan.
authors.forename: Robert L
authors.initials: RL
authors.lastname: Hammond
authors.affiliation: Department of Physiology and Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan.
authors.forename: Abhinav C
authors.initials: AC
authors.lastname: Krishnan
authors.affiliation: Department of Physiology and Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan.
authors.forename: Alberto
authors.initials: A
authors.lastname: Alvarez
authors.affiliation: Department of Physiology and Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan.
authors.forename: Robert A
authors.initials: RA
authors.lastname: Augustyniak
authors.affiliation: Department of Physiology and Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan doleary@med.wayne.edu.
authors.forename: Donal S
authors.initials: DS
authors.lastname: O'Leary
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists / Q000494:pharmacology; D058672:Adrenergic beta-2 Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D004837:Epinephrine / Q000097:blood*; D005260:Female; D006614:Hindlimb / Q000098:blood supply / Q000502:physiology; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply / Q000187:drug effects / Q000502:physiology; D005082:Physical Exertion; D011224:Prazosin / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D012018:Reflex; D012039:Regional Blood Flow; D014664:Vasodilation
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D058672:Adrenergic beta-2 Receptor Antagonists; D011433:Propranolol; D011224:Prazosin; D004837:Epinephrine
keywords: epinephrine; exercise pressor reflex; β2-adrenergic vasodilation