Baroreflex regulation of sympathetic neuronal discharge during large, rapid changes in blood pressure caused by ventricular bigeminy and sinus pause.

This study investigated baroreflex regulation of sympathetic action potential (AP) discharge during large, rapid blood pressure changes caused by ventricular bigeminy and sinus pause in a healthy female participant. Muscle sympathetic APs (microneurography, continuous wavelet transform) and blood pressure (Finometer) were recorded during baseline (BSL; 5-min), cold face challenge (Cold; 0°C cold pack), and a maximal end-inspiratory apnea. Cold face challenge increased sympathetic AP discharge (BSL: 8 APs/burst, Cold: 49 APs/burst) and recruited large APs (BSL: 21 AP clusters, Cold: 27 AP clusters). Ventricular bigeminy occurred during cold face challenge and caused large increases in mean pressure (+16 mmHg). The first bigeminal beat reduced sympathetic AP discharge (bigeminy beat 1: 7 APs/burst) and derecruited large APs (bigeminy beat 1: 4 AP clusters). As bigeminy continued (bigeminy beats 2 and 3) and blood pressure remained high, AP discharge increased (bigeminy beats 2 and 3 average: 43 APs/burst), and large APs were rerecruited (bigeminy beats 2 and 3 average: 18 AP clusters). During bigeminy, sympathetic AP baroreflex functions were reset upward to higher discharge probabilities and rightward to higher blood pressures, indicating rapid baroreflex resetting. Bigeminy also reduced sympathetic AP discharge latency (-0.04 s). During a separate apnea protocol, a 2.4-s sinus pause occurred and caused a large reduction in mean pressure (-15 mmHg) that increased the discharge of medium- and large-sized sympathetic APs. This experiment of nature, enabled by ventricular bigeminy and sinus pause, suggests that the baroreflex governs sympathetic AP discharge, recruitment, and latency during large, rapid blood pressure changes.NEW & NOTEWORTHY Our knowledge regarding human baroreflex regulation of sympathetic action potential (AP) discharge remains incomplete. Cardiac arrhythmias in a healthy female provided a unique opportunity to examine baroreflex regulation of sympathetic AP discharge during large, rapid blood pressure changes. Our novel findings include: 1) rapid baroreflex loading due to ventricular bigeminy reduced AP discharge and derecruited large APs, 2) as bigeminy continued, rapid baroreflex resetting increased AP discharge, and 3) rapid baroreflex loading reduced AP latency.