Impact of swimming exercise on inflammation in medullary areas of sympathetic outflow control in spontaneously hypertensive rats.

Exercise reduces sympathetic activity (SA), arterial pressure and heart rate in spontaneously hypertensive rats (SHR). Exercise increases oxidative stress (OS) and inflammation is implicated in the generation of reactive oxygen species (ROS) and progression of hypertension. To unravel these effects of exercise and considering that SA is driven by medullary areas, we hypothesized that swimming exercise (SW) affects the gene expression (g.e.) of proteins involved in inflammation and OS in the commissural Nucleus of the Solitary Tract (cNTS) and Rostral ventrolateral medulla (RVLM), which control the sympathetic outflow in SHR. We used male SHR and Wistar rats (14-16wks-old) which were maintained sedentary (SED) or submitted to SW (1 h/day, 5 days/wk./6wks). The g.e. of cycloxygenase-2 (COX-2), interleukin 6 (IL-6), interleukin 10 (IL-10), AT-1 receptor (AT-1r), neuroglobin (Ngb) and cytoglobin (Ctb) in cNTS and RVLM was carried out by qPCR. We observed that COX-2 g.e. increased in SW-SHR in cNTS and RVLM compared to SED-SHR. The IL-6 g.e. reduced in RVLM in SW-SHR, whereas IL-10 g.e. increased in SW-SHR in comparison to SED-SHR. The AT-1r g.e. decreased in SW-SHR in cNTS and RVLM compared to SED-SHR. The Ngb and Ctb g.e. in cNTS neurons increased in SHR and Wistar rats submitted to SW compared to SED, but only Ctb g.e. increased in RVLM in SW-SHR and Wistar in comparison to SED. Therefore, the SW altered the g.e. in cNTS and RVLM for reducing the inflammation and ROS formation, which is increased particularly in SHR, consequently decreasing the OS.