Severs, W.B., J.Y. Summy-Long, and L.C. Keil: The brain renin-angiotensin system. Drug Dev. Res: 2:231-239, 1982. Considerable evidence suggests that angiotensin interacts with the central nervous system (CNS) to increase blood pressure and alter peripheral hydration. Blood-borne angiotensin may affect circumventricular organs resulting in increased water intake and vasopressin release. In addition, current literature documents the presence of a complete renin-angiotensin system (RAS) in the brain. Angiotensin, presumably of central origin, increases sodium excretion; an effect opposite to blood-borne peptide. This effect, along with increased water turnover, could dilute body fluids. The relative activities of the peripheral (renal) and central RASs thus may be of considerable importance in both normal and pathophysiological control of blood pressure and hydration. Indeed, some models of spontaneous hypertension in rats are associated with an altered brain RAS; central administration of converting enzyme inhibitors or angiotensin receptor antagonists returns elevated blood pressure toward normal.