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Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801
The cardiovascular responses induced by exercise are initiated by two primary mechanisms: central command and reflexes originating in exercising muscles. Although our understanding of cardiovascular responses to exercise in mice is progressing, a murine model of cardiovascular responses to muscle contraction has not been developed. Therefore, the purpose of this study was to characterize the cardiovascular responses to muscular contraction in anesthetized mice. The results of this study indicate that mice demonstrate significant increases in blood pressure (13.8 ± 1.9 mmHg) and heart rate (33.5 ± 11.9 beats/min) to muscle contraction in a contraction-intensity-dependent manner. Mice also demonstrate 23.1 ± 3.5, 20.9 ± 4.0, 21.7 ± 2.6, and 25.8 ± 3.0 mmHg increases in blood pressure to direct stimulation of tibial, peroneal, sural, and sciatic hindlimb somatic nerves, respectively. Systemic hypoxia (10% O2-90% N2) elicits increases in blood pressure (11.7 ± 2.6 mmHg) and heart rate (42.7 ± 13.9 beats/min), while increasing arterial pressure with phenylephrine decreases heart rate in a dose-dependent manner. The results from this study demonstrate the feasibility of using mice to study neural regulation of cardiovascular function during a variety of autonomic stimuli, including exercise-related drives such as muscle contraction.
mouse; muscle contraction; pressor reflex; genetic; hypoxia
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