Contribution of retrotrapezoid nucleus neurons to CO 2 ‐amplified cardiorespiratory activity in spontaneously hypertensive rats

Key points This study demonstrates that both CO 2 ‐induced respiratory and cardiovascular responses are augmented in spontaneously hypertensive rats (SHRs). Genetic ablation of the retrotrapezoid nucleus (RTN) neurons depresses enhanced hypercapnic ventilatory response eliminates ‐stimulated increase arterial pressure heart rate SHRs. SHRs have a high protein level pH‐sensitive channels RTN, including TASK‐2 channel, Kv12.1 channel acid‐sensing ion 3. The inhibition putative activity by clofilium diminishes amplified responses, reduces number ‐activated RTN These results indicate contribute to Abstract regulation is essential for maintaining an efficient ventilation perfusion ratio. Activation central chemoreceptors not only elicits but also regulates sympathetic nerve blood (ABP). most completely characterized cluster chemoreceptors. We hypothesize adult Our findings exhibit more cardiorespiratory than age‐matched normotensive Wistar–Kyoto rats. notably (HCVR) greater ABP In addition, higher channels, Administration ( i.p. ), unselective inhibitor significantly HCVR inhibits ‐amplified increases Moreover, decreases Taken together, we suggest play important role mechanism involved associated with RTN.