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1 Physiology, Wayne State University School of Medicine, Detroit, MI, USA
2 Physiology, Wayne State University School of Medicine, Detroit, MI, USA; Surgery, Wayne State University School of Medicine, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: doleary{at}med.wayne.edu.
Previous studies have shown that heart failure (HF) or sino-aortic denervation (SAD) alters the strength and mechanisms of the muscle metaboreflex during dynamic exercise. However, it is still unknown to what extent SAD may modify the muscle metaboreflex in HF. Therefore, we quantified the contribution of cardiac output (CO) and peripheral vasoconstriction to metaboreflex-mediated increases in mean arterial blood pressure (MAP) in conscious, chronically instrumented dogs before and after induction of HF in both barointact and SAD conditions during mild and moderate exercise. The muscle metaboreflex was activated via partial reductions in hindlimb blood flow. After SAD, the metaboreflex pressor responses were significantly higher with respect to barointact condition despite lower CO responses. The pressor response was significantly lower in HF after SAD but still higher than that of HF in barointact condition. During control experiments in barointact condition, total vascular conductance summed from all beds except the hindlimbs did not change with muscle metaboreflex activation, whereas in the SAD condition both before and after induction of HF significant vasoconstriction occurred. We conclude that SAD substantially increased the contribution of peripheral vasoconstriction to metaboreflex-induced increases in MAP, whereas in HF, SAD did not markedly alter the patterns of the reflex responses likely reflecting that in HF, the ability of the arterial baroreflex to buffer metaboreflex responses is impaired.
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