Key result
Vagotomy increases sympathetic nerve activity in normal but not HF rats, reflecting lost vagal modulation.
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Loss of vagal baroreflex modulation may drive sympathetic overactivity in HF; extends mechanistic insights from animal models but leaves translation open.
The arterial baroreflex system can be divided into the neural arc, from pressure input to efferent sympathetic nerve activity (SNA), and the peripheral arc, from SNA to arterial pressure (AP). Plotting the neural and peripheral arcs on a pressure-SNA plane yields a baroreflex equilibrium diagram. We examined the effects of vagotomy on the open-loop static characteristics of the carotid sinus baroreflex in normal control rats (NC, n = 10) and rats with heart failure after myocardial infarction (MI, n = 10). In the NC group, vagotomy shifted the neural arc toward higher SNA and decreased the slope of the peripheral arc. Consequently, the operating-point SNA increased without a significant change in the operating-point AP on the baroreflex equilibrium diagram. These vagotomy-induced effects were not observed in the MI group, suggesting a loss of vagal modulation of the carotid sinus baroreflex function in heart failure.
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Kawada et al. (2016) studied Chronic Heart Failure (n=20). Vagotomy vs. Normal control rats was evaluated on Open-loop static characteristics of the carotid sinus baroreflex. Vagotomy increased operating-point sympathetic nerve activity in normal rats but not in rats with heart failure, indicating a loss of vagal modulation of baroreflex function in heart failure.
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