Abstract

A single bout of dynamic exercise lowers blood pressure in hypertensive subjects, named post‐exercise hypotension (PEH). We previously showed that exercise reduced GABA release in the NTS. Within the NTS, the balance of excitatory and inhibitory synaptic transmissions is integrated into the intrinsic excitability of baroreceptive neurons to shape baroreflex output from the NTS to downstream synapses. Here, I tested the hypothesis that a single exercise bout increases intrinsic excitability and excitatory synaptic inputs in NTS 2nd‐order baroreceptive neurons. Resting membrane potential (Rem), spiking response to depolarization, inwardly‐rectified K currents (Kir), spontaneous excitatory postsynaptic currents (sEPSCs), and miniature EPSCs were recorded in anatomically identified 2nd‐order baroreceptive neurons in a brainstem slice. Neurons from the PEH group (n=10) had a slightly depolarized Rem and significantly higher spiking activity (p<0.05) at Rem. When the neurons were current‐clamped at ‐60 mV there was no significant difference in spiking activity or spiking response to depolarization between sham and PEH. In addition, Kir currents were smaller in neurons from the PEH group. Neurons from the PEH group (n=7) also had higher sEPSC and mEPSC frequencies (p<0.05). Data suggest that increased intrinsic and synaptic excitability of NTS 2nd‐order baroreceptive neurons may contribute to the PEH.

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