Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature

• Published in: Journal of applied physiology (1985) Vol. 103; no. 1; pp. 190 - 194
• Main Authors: O'Leary, Donal S, Sala-Mercado, Javier A, Hammond, Robert L, Ansorge, Eric J, Kim, Jong-Kyung, Rodriguez, Jaime, Fano, Dominic, Ichinose, Masashi
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Physiological Soc 01.07.2007; American Physiological Society
• Subjects: Adrenergic alpha-1 Receptor Antagonists; Adrenergic alpha-Antagonists - pharmacology; Animals; Biological and medical sciences; Blood Flow Velocity; Blood Pressure; Cardiac Output; Coronary Circulation; Coronary vessels; Coronary Vessels - drug effects; Coronary Vessels - innervation; Dogs; Exercise; Fundamental and applied biological sciences. Psychology; Heart - drug effects; Heart - innervation; Heart Rate; Muscle Contraction; Muscle, Skeletal - blood supply; Muscle, Skeletal - drug effects; Muscle, Skeletal - innervation; Muscle, Skeletal - metabolism; Musculoskeletal system; Physical Exertion - physiology; Prazosin - pharmacology; Receptors, Adrenergic, alpha-1 - metabolism; Reflex - drug effects; Regional Blood Flow; Sympathetic Nervous System - drug effects; Sympathetic Nervous System - physiology; Vasoconstriction - drug effects; Ventricular Function - drug effects; Physical exercise; α-adrenergic receptors; Quinazoline derivatives; ventricular function; α1-Adrenergic receptor; Cardiovascular disease; Striated muscle; Sympathetic nervous system; Coronary heart disease; Blood flow; Prazosin; Vertebrata; Alpha blocking agent; Mammalia; Metaboreflex; Autonomic nervous system; α-Adrenergic receptor; exercise pressor response; Antagonist; Hemodynamics; coronary blood flow
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00139.2007

Departments of 1 Physiology and 2 Surgery, Wayne State University School of Medicine, Detroit, Michigan; and 3 Laboratory for Applied Human Physiology, Faculty of Human Development, Kobe University, Kobe, Japan Submitted 1 February 2007 ; accepted in final form 23 April 2007 Ischemia of active skeletal muscle evokes a powerful blood pressure-raising reflex termed the muscle metaboreflex (MMR). MMR activation increases cardiac sympathetic nerve activity, which increases heart rate, ventricular contractility, and cardiac output (CO). However, despite the marked increase in ventricular work, no coronary vasodilation occurs. Using conscious, chronically instrumented dogs, we observed MMR-induced changes in arterial pressure, CO, left circumflex coronary blood flow (CBF), and coronary vascular conductance (CVC) before and after 1 -receptor blockade (prazosin, 100 µg/kg iv). MMR was activated during mild treadmill exercise by partially reducing hindlimb blood flow. In control experiments, MMR activation caused a substantial pressor response-mediated via increases in CO. Although CBF increased (+28.1 ± 3.7 ml/min; P < 0.05), CVC did not change (0.45 ± 0.05 vs. 0.47 ± 0.06 ml·min –1 ·mmHg –1 , exercise vs. exercise with MMR activation, respectively; P > 0.05). Thus all of the increase in CBF was due to the increase in arterial pressure. In contrast, after prazosin, MMR activation caused a greater increase in CBF (+55.9 ± 17.1 ml/min; P < 0.05 vs. control) and CVC rose significantly (0.59 ± 0.08 vs. 0.81 ± 0.17 ml·min –1 ·mmHg –1 , exercise vs. exercise with MMR activation, respectively; P < 0.05). A greater increase in CO also occurred (+2.01 ± 0.1 vs. +3.27 ± 1.1 l/min, control vs. prazosin, respectively; P < 0.05). We conclude that the MMR-induced increases in sympathetic activity to the heart functionally restrain coronary vasodilation, which may limit increases in ventricular function. exercise pressor response; coronary blood flow; ventricular function; prazosin; -adrenergic receptors Address for reprint requests and other correspondence: D. S. O'Leary, Dept. of Physiology, Wayne State Univ. School of Medicine, 540 E. Canfield Ave, Detroit, MI 48201 (e-mail: doleary{at}med.wayne.edu )