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1 Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA
2 Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA; Department of Surgery, Wayne State University School of Medicine, Detroit, MI, USA
3 Deparment of Internal Medicine, Wayne State University School of Medicine, Detroit, MI, USA; John D. Dingell Veterans Administration Medical Center, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: doleary{at}med.wayne.edu.
Arterial baroreflex function is well preserved during dynamic exercise in normal subjects. In subjects with heart failure (HF), arterial baroreflex ability to regulate blood pressure is impaired at rest. However, whether exercise modifies the strength and mechanisms of baroreflex responses in HF is unknown. Therefore, we investigated the relative roles of cardiac output (CO) and peripheral vasoconstriction in eliciting the pressor response to bilateral carotid occlusion (BCO) in conscious, chronically instrumented dogs at rest and during treadmill exercise ranging from mild to heavy workloads. Experiments were performed in the same animals before and after rapid ventricular pacing-induced HF. At rest, the pressor response to BCO was significantly attenuated in HF (33.3 ± 1.2 vs. 18.7 ± 2.7 mmHg) and this difference persisted during exercise in part due to lower CO responses in HF. However, both before and after induction of HF, the contribution of vasoconstriction in active skeletal muscle towards the pressor response became progressively greater as workload increased. We conclude that although there is impaired ability of the baroreflex to regulate arterial pressure at rest and during exercise in HF, vasoconstriction in active skeletal muscle becomes progressively more important in mediating the baroreflex pressor response as workload increases with a pattern similar to that observed in normal subjects.
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