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benefits opening the possibility for its usage in the clinical practice. For instance,
clinical studies demonstrated that central autonomic adaptations induced by aerobic
training are the main cause of baroreflex sensitivity improvement in hypertensive
patients [ 1 ]. Indeed, experimental studies in spontaneously hypertensive rats (SHR)
identified that normalization of baroreflex function and improvement of cardiac
vagal activity are timely correlated with both the downregulation of brain renin-
angiotensin system and the reduction of oxidative stress and inflammatory profile in
autonomic control areas [ 2 , 3 ]. The present chapter, reviewing these data and others
focused in the cross-talking between tissue dysfunction and molecular/cellular
responses, allows the physical training prescribers to understand the physiological
mechanisms that attenuate autonomic dysfunction and how the improvement of
autonomic regulation contributes to a better circulatory control in hypertension.
2 Central Nervous System and Autonomic Dysfunction
in Hypertension
Directly coupled to cardiovascular system, central nervous system drives both acute
and chronic hemodynamic adjustments during distinct environmental conditions.
For this purpose, the brain continuously monitors the cardiovascular parameters and
integrates these signals in order to reflexly codify cardiovascular and metabolic
parameters through the sympathetic and parasympathetic divisions of the autonomic
nervous system. There are three major sets for afferent signaling of cardiovascular
parameters: arterial baroreceptors, peripheral chemoreceptors and cardiopulmonary
receptors. These intrinsic receptors of the cardiovascular system codify pressure
levels, circulating blood gases and cardiac function, respectively, whose signals are
integrated in central autonomic areas, triggering appropriate parasympathetic and
sympathetic outflow to heart and vessels [ 4 , 5 ]. In hypertension, peripheral signal-
ing mainly by baroreceptors and chemoreceptors are dysfunctional and central inte-
grative autonomic mechanisms are abnormal, contributing to increased sympathetic
nerve activity and suppressed parasympathetic nerve activity, which characterizes
the concept of autonomic dysfunction [ 6 – 8 ].
Baroreflex is recognized as the most important beat-to-beat regulatory mecha-nism of arterial pressure. Baroreceptors are located in the adventitial and media
tunica of aortic arch and carotid sinus. These mechanoreceptors present channels of
Degenerin/Epithelial Na + channel, Acid sensing ion channel 2 [ 9 ], and transient
receptor potential cations channels superfamilies, as the transient receptor potential
channel 5 [ 10 ]. Once the pressure wave strains the vascular wall in the aortic arch
and carotid sinus, the baroreceptors are stretched and the mechanosensitive chan-
nels induce a cationic influx, which depolarizes Na + channels and increases aortic
depressor nerve activity. In the brainstem, second order neurons located at nucleus
tractus solitarii (NTS) are stimulated, activating parasympathetic areas, as the nucleus
ambiguus (NA) and the dorsal nucleus of vagus nerve (DMV) [ 4 ]. Also, these
G.S. Masson and L.C. Michelini