Exercise pressor reflex (EPR) induced FOS expression is co‐localized with neurons containing neuronal nitric oxide synthase (nNOS) in the nucleus tractus solitarius (NTS)

The pressor response to stimulation of the skeletal muscle EPR is exaggerated in hypertension (HTN). EPR sensory neurons relay information from contracting muscle to the NTS in the brainstem. The protein nNOS is present in the NTS and produces nitric oxide (NO). NO buffers the pressor response to EPR activation. Previously, we determined that nNOS expression is reduced in the medial NTS of spontaneously hypertensive rats (SHR). This suggests that decreases in nNOS mediated NO production in the NTS could contribute to EPR overactivity in HTN. However, it is still unknown whether neurons excited by the EPR contain nNOS or are in close proximity to neurons that express nNOS. In SHR and normotensive rats, the EPR was rhythmically activated by electrically induced hindlimb muscle contraction for one hour. Neurons excited by the EPR transcribe FOS, a product of the early response gene c‐ fos . FOS expression delineates EPR induced neuronal excitation. Brainstem tissue was stained for FOS and nNOS. Using confocal microscopy, it was determined that, lateral to the calamus scriptorius within the medial NTS, EPR induced FOS expression was co‐localized with neurons containing nNOS. Combined with our previous findings, this study provides anatomical evidence supporting the concept that EPR overactivity in HTN is mediated by reductions in NO production via nNOS in the NTS. Supported by NIH HL‐088422