Central chemoreflex activation induces sympatho‐excitation without altering static or dynamic baroreflex function in normal rats

Central chemoreflex activation induces sympatho‐excitation. However, how central chemoreflex interacts with baroreflex function remains unknown. This study aimed to examine the impact of central chemoreflex on the dynamic as well as static baroreflex functions under open‐loop conditions. In 15 anesthetized, vagotomized Sprague‐Dawley rats, we isolated bilateral carotid sinuses and controlled intra‐sinus pressure ( CSP ). We then recorded sympathetic nerve activity ( SNA ) at the celiac ganglia, and activated central chemoreflex by a gas mixture containing various concentrations of CO 2 . Under the baroreflex open‐loop condition ( CSP  = 100 mmHg), central chemoreflex activation linearly increased SNA and arterial pressure ( AP ). To examine the static baroreflex function, we increased CSP stepwise from 60 to 170 mmHg and measured steady‐state SNA responses to CSP (mechanoneural arc), and AP responses to SNA (neuromechanical arc). Central chemoreflex activation by inhaling 3% CO 2 significantly increased SNA irrespective of CSP , indicating resetting of the mechanoneural arc, but did not change the neuromechanical arc. As a result, central chemoreflex activation did not change baroreflex maximum total loop gain significantly (−1.29 ± 0.27 vs. −1.68 ± 0.74, N.S.). To examine the dynamic baroreflex function, we randomly perturbed CSP and estimated transfer functions from 0.01 to 1.0 Hz. The transfer function of the mechanoneural arc approximated a high‐pass filter, while those of the neuromechanical arc and total ( CSP ‐ AP relationship) arcs approximated a low‐pass filter. In conclusion, central chemoreflex activation did not alter the transfer function of the mechanoneural, neuromechanical, or total arcs. Central chemoreflex modifies hemodynamics via sympatho‐excitation without compromising dynamic or static baroreflex AP buffering function.