Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature.
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 alpha1-receptor blockade (prazosin, 100 microg/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 x min(-1) x 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 x min(-1) x 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.
O'Leary
Donal S
DS
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA. doleary@med.wayne.edu
Sala-Mercado
Javier A
JA
Hammond
Robert L
RL
Ansorge
Eric J
EJ
Kim
Jong-Kyung
JK
Rodriguez
Jaime
J
Fano
Dominic
D
Ichinose
Masashi
M
D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002302:Cardiac Output; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000187:drug effects / Q000294:innervation*; D004285:Dogs; D006321:Heart / Q000187:drug effects / Q000294:innervation*; D006339:Heart Rate; D009119:Muscle Contraction; D018482:Muscle, Skeletal / Q000098:blood supply / Q000187:drug effects / Q000294:innervation* / Q000378:metabolism; D005082:Physical Exertion / Q000502:physiology*; D011224:Prazosin / Q000494:pharmacology; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism; D012018:Reflex / Q000187:drug effects; D012039:Regional Blood Flow; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects; D016276:Ventricular Function / Q000187:drug effects
D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; D018340:Receptors, Adrenergic, alpha-1; D011224:Prazosin