Afferent vagal nerve stimulation induced sympathoinhibition may in part attribute to the beneficial impact of vagal nerve stimulation on heart failure

Purpose: Although the augmented sympathetic nerve activity (SNA) is a salient feature of heart failure, while vagal nerve stimulation (VNS) benefits patients with heart failure. How the VNS impacts on SNA remains unknown. Since the vagal trunk has both efferent and afferent fibers, we hypothesized that the vagal afferent stimulation (AVNS) impacts on baroreflex control of SNA. Methods and results: In 6 anesthetized, ventilated rats, we controlled the pressure of isolated, bilateral carotid sinuses (CSP) and measured celiac SNA and arterial pressure (AP). Under a constant CSP at 100 mmHg, increasing the voltage of AVNS captured the vagal afferent nerves at 2-4 volts and dose dependently decreased SNA and AP. The averaged maximal inhibition of SNA were -27.3±5.3% (Fig. 1). To examine the impact of AVNS on the baroreflex system, we changed CSP stepwise and measured the response of SNA and AP with/without AVNS. AVNS reset the sigmoidal CSP-SNA relation (neural arc) downward, whereas unaffected the linear SNA-AP relation (peripheral arc) (Fig. 2). To evaluate the dynamic impacts of AVNS on SNA, we randomly stimulated AVNS with binary white noise sequences, and identified the transfer function from AVNS to SNA and that from SNA to AP. We also identified transfer function of native baroreflex from CSP to SNA and from SNA to AP. The transfer functions from AVNS to SNA strikingly resembled that from CSP to SNA. The transfer functions from SNA to AP were indistinguishable whether we perturbed CSP or AVNS indicating that they share the common central and peripheral neural mechanism. ![Figure][1] Conclusions: AVNS resets the baroreflex neural arc and induces sympathoinhibition just like the native baroreflex. The AVNS induced sympathoinhibition may in part attribute to the beneficial impacts of VNS on heart failure. [1]: pending:yes