Abstract
A possible role of brain angiotensin II (A-II) and angiotensin receptors within the central nervous system in the development of hypertension was first suggested in 1961 (1) and since then, investigators have identified every component of the renin-angiotensin system to be present within the brain (2). The chronic intraventricular (IVT) administration of A-II to awake dogs for 2 to 4 weeks has been reported to produce sustained hypertensive effects only if the daily intake of sodium is increased (3). This present study was undertaken to investigate the effects of chronic administration of renin, 0.15 Goldblatt units (Gu) IVT twice daily to awake instrumented dogs and to determine if an increase in the daily intake of sodium is necessary for physiological and/or pathological effects to be produced by the endogenous increase of A-II within the cerebrospinal fluid.