Muscle metaboreflex elicits α1 adrenergic vasoconstriction in the coronary vasculature

• Published in: The FASEB journal 2006-03, Vol.20 (4), p.A769-A769
• Main Authors: O’Leary, Donal S., Hammond, Robert L., Sala‐Mercado, Javier A., Ansorge, Eric A., Kim, Jong‐Kyung, Rodriguez, Jaime, Fano, Dominic
• Format: Article
• Language: English
• ISSN: 0892-6638; 1530-6860
• DOI: 10.1096/fasebj.20.4.A769

Ischemia in active skeletal muscle activates afferents which induces a reflex pressor response, termed the muscle metaboreflex (MMR). MMR activation during submaximal treadmill exercise elicits substantial increases in heart rate and cardiac output (CO), in part, via increases in efferent cardiac sympathetic activity. We investigated whether this increase in sympathetic tone functionally vasoconstricts the coronary vasculature. Six dogs were chronically instrumented to measure CO, mean arterial pressure (MAP) and left circumflex coronary blood flow (CBF). MMR was activated during mild treadmill exercise (3.2 km/h) via imposed partial reductions in hindlimb blood flow (~50%). Experiments were performed before and after systemic α1 adrenergic receptor blockade (prazosin 100 μg/kg, i.v.). In control experiments MMR activation caused substantial increases in MAP (+42 ± 5 mmHg) and CO (+1.6 ± 0.3 l/min). However, no significant change in coronary vascular conductance (CVC) occurred despite that cardiac work rose markedly (a substantially higher CO pumped against a higher pressure). In contrast, with MMR activation after α1 adrenergic receptor blockade, CVC significantly increased (+33 ± 9 %) and the rise in CO (+3.0 ± 0.56 l/min) was also significantly greater. We conclude that MMR‐induced increases in sympathetic activity to the heart functionally restrains coronary vasodilation which may limit increases in ventricular performance. HL‐55473 and IMSD grant GM 58905