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carotid artery [ 6 ]. Thus, the afferent signals of the baroreceptors in the peripheral
system trigger the release of a signal from the nucleus tractus solitarius in the
medulla with twofold destination: decrease of the heart rate through parasympa-
thetic vagal stimulation and lowering of blood pressure through tonic inhibition of
neurons in the rostral ventrolateral medulla, with the intervention of non-
catecholaminergic depressor neurons in caudal ventrolateral medulla. It is currently
believed that the sympathetic over-activation in RH is generated by a disproportion
between the catecholaminergic neurons in the brain stem and decrease or even loss
of the inhibitory function of the non-catecholaminergic neurons in the rostral and
caudal ventrolateral medulla; however, this hypothesis has not been directly inves-
tigated [ 7 ].
Another involvement of rostral ventrolateral medulla in RH genesis is neurovas-
cular compression induced by the posterior inferior cerebellar artery and vertebral
artery. This process causes loss of the same inhibitory effect on blood pressure,
mainly transmitted via vagus and glossopharyngeal nerves. Thus, sympathetic nerve
activity, arterial pressure, heart rate, and plasma levels of epinephrine and norepi-
nephrine were increased by pulsatile compression of these neurons [ 8 ].
Furthermore, the “adrenaline hypothesis” currently still under debate takes into
account the role of neurotransmitter in the self-maintenance of essential hyperten-
sion, through a positive feedback loop developed at the level of the presynaptic
beta-adrenoceptors [ 9 ].
Vagal Modulation
Since hypertension is characterized by an increased sympathetic tone, the evalua-
tion of the sympathovagal balance could ascertain more accurately the possibility
that vagal tone could also be involved in RH pathogenesis. Rhythmic components
of heart rate variability (HRV, evaluated by RR interval recordings) permit to evalu-
ate autonomic activity at baseline conditions and to separate the different compo-
nents of variability which seem to reflect specific regulatory mechanisms. The
high-frequency (HF) component is a marker of vagal activity, while the low-
frequency (LF) component is a marker of sympathetic and vagal activity. The LF/
HF ratio is considered as a marker of sympathovagal balance [ 10 , 11 ].
It is a known fact that vagal nerves influence blood pressure variability more than
the sympathetic system [ 12 ]. Moreover, blood pressure variability is related to vari-
ability of heart rate which is largely influenced by vagal tone [ 13 ].
Therapeutic correlation Modulating parasympathetic system by direct vagal nerve
stimulation is an emerging interventional therapy [ 14 ]. A recent study using a new
technique of tripolar stimulation decreased blood pressure in rats without inadver-
tent stimulation of non-baroreceptive fibers (reducing the side effects like bradycar-
dia and bradypnea) [ 15 ].
A. Burlacu and A. Covic