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BM-derived cells in neuroinflammation is currently being investigated. Experimental
evidence indicates that minocycline, an inhibitor of microglial activation, could rep-
resent an effective therapy due to its ability to alter neurogenic components of
hypertension.
Renalase
Several researches unveiled a new mechanism involved in regulation of cardiac
function and blood pressure: the renalase pathway. Renalase is an amine oxidase
synthetized in the kidney, inactive at baseline, which metabolizes circulating cate-
cholamines. Its activation is very swift, and it is triggered by any small variation in
blood pressure and plasma catecholamines, leading to an important decrease in
blood pressure [ 34 ]. Damages in synthesis of renalase are connected with elevated
blood pressure and increases in circulating catecholamines. Currently, the mecha-
nisms responsible for the involvement of renalase deficiency in hypertension, as
well as the possible contribution of renalase to the regulation of renal dopamine
system, are not well described [ 35 ].
Gut Microbiota
Recent research on Dahl rats have proven the correlation between gut microbial
content and blood pressure regulation, with further perspectives opened for investi-
gation regarding the possible association between the host genome and microbiome
within the context of blood pressure regulation [ 36 ].
GABAA Receptors
Studies on BPH/2J mice demonstrated the cardiovascular effects of chronic activa-
tion of GABAA receptors. It seems that their impairment may play a role in the
mechanism of neurogenic hypertension by the failure to suppress arousal-induced
sympathetic activation within the amygdala and hypothalamic nuclei [ 37 ].
RAAS Mechanisms
Angiotensin-Aldosterone Escape Pathway
The mechanisms underlying the renin-angiotensin-aldosterone system (RAAS)
have been extensively investigated and described. However, recent research has
ascertained that the processes are much more complex than a straightforward
A. Burlacu and A. Covic