“…Prolongation of this disorder leads to exhaustion of DR-5HT but not MR-5HT neurons thus, predominance of the latter occurs during chronic stress situation. A bulk of information dealing with this issue has been quoted and affords support for the postulation that this pathophysiological mechanism should underlies in many diseases, like endogenous depression (Beaulieu et al, 1986;Lechin et al, 2006a,), TH-1 autoimmune diseases and EH, all of which frequently show exhaustion of adrenal glands activity plus disinhibition of the thymus gland secondary to the lowered levels of circulating cortisol (Herman et al, 2005;Huether 1996;Huether et al, 1996;Lovick 1993;Robinson et al, 1983). Summarizing all the above, DR-5HT hyperactivity is able to trigger labile hypertensive syndromes by the enhancement of the acute stress mechanisms but this type of physiological disorder travels in the opposite address of that which leads to the disorder underlying EH.…”