Beschreibung:
<jats:p>The renin-angiotensin system (RAS), originally described as a circulating hormone system, is an enzymatic cascade in which the final vasoactive peptide angiotensin II (ANG) regulates cardiovascular, hydromineral, and metabolic functions. The RAS is also synthesized locally in a number of tissues including the brain, where it can act in a paracrine fashion to regulate blood pressure, thirst, fluid balance, and resting energy expenditure/resting metabolic rate (RMR). Recent studies demonstrate that ANG AT<jats:sub>1A</jats:sub>receptors ( Agtr1a) specifically in agouti-related peptide (AgRP) neurons of the arcuate nucleus (ARC) coordinate autonomic and energy expenditure responses to various stimuli including deoxycorticosterone acetate (DOCA)-salt, high-fat feeding, and leptin. It remains unclear, however, how these disparate stimuli converge upon and activate this specific population of AT<jats:sub>1A</jats:sub>receptors in AgRP neurons. We hypothesize that these stimuli may act to stimulate local expression of the angiotensinogen (AGT) precursor for ANG, or the expression of AT<jats:sub>1A</jats:sub>receptors, and thereby local activity of the RAS within the (ARC). Here we review mechanisms that may control AGT and AT<jats:sub>1A</jats:sub>expression within the central nervous system, with a particular focus on mechanisms activated by steroids, dietary fat, and leptin.</jats:p>