Submitted on February 1, 2007
Accepted on April 25, 2007
Muscle metaboreflex induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature
Donal S O'Leary1*, Javier A Sala-Mercado1, Robert L Hammond2, Eric J. Ansorge1, Jong-Kyung Kim3, Jaime Rodriguez3, Dominic Fano4, and Masashi Ichinose4
1 Department of Physiology, Wayne State University, Detroit, Michigan, United States
2 Surgery, Wayne State University, Detroit, Michigan, United States
3 Physiology, Wayne State University, Michigan, United States
4 Physiology, Wayne State University, 48201, Michigan, United States
* To whom correspondence should be addressed. E-mail: doleary{at}med.wayne.edu.
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 alpha 1 receptor blockade (prazosin, 100µg/kg, i.v.). 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/mmHg, P > 0.05, exercise vs. exercise with MMR activation, respectively). 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/mmHg, P < 0.05, exercise vs. exercise with MMR activation, respectively). A greater increase in CO also occurred (+2.01 ± 0.1 vs. +3.27 ± 1.1 l/min, P < 0.05 control vs. prazosin, respectively) . We conclude that the MMR induced increases in sympathetic activity to the heart functionally restrain coronary vasodilation which may limit increases in ventricular function.
