A recent study published in Hypertension demonstrates that cytokines such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α acting at the level of the subfornical organ induce the expression of inflammatory and excitatory mediators that subsequently drive sympathetic nervous system activation.
The subfornical organ (SFO), a highly vascularized structure is a circumventricular organ that lacks a blood–brain barrier. Previous research indicates this brain structure is a crucial ‘sensor’ for peripheral inflammation, mediating the central effects of certain pro-inflammatory cytokines, and thus, contributing to an increase in autonomic and neuro-hormonal output.
In the Hypertension study Shun-Guang Wei and colleagues from the University of Iowa Carver College of Medicine, Iowa City, IA provide evidence that IL-1β and TNF-α up-regulate mediators and mechanisms that increase the brain renin–angiotensin system (RAS) activity or prostaglandin E2 production in the SFO of male Sprague–Dawley rats.
The SFO is directly exposed to blood-borne signals and peripheral cytokines, and it projects straight to the cardiovascular autonomic nuclei.
The authors suggest that through the above mentioned effects and mechanisms, peripheral pro-inflammatory cytokines are able to drive a chronic and sustained hyperactivity of the sympathetic nervous system observed in pathologic states such as heart failure or some forms of hypertension.
In addition, according to the authors, these mechanisms and pathogenic loops can be amplified by other excitatory mediators, like angiotensin II and aldosterone that circulate in chronic states like heart failure and hypertension.