In addition to its extrarenal functions, including the control of arterial pressure and aldosterone secretion, the renin-angiotensin system (RAS) also has multiple intrarenal actions in controlling glomerular filtration rate (GFR) and sodium excretion. Angiotensin II (AngII) helps to prevent excessive decreases in GFR in different physiological and pathophysiological conditions by preferentially constricting the efferent arterioles, an action that can be mediated by either intrarenally formed or circulating AngII. Circulating AngII and intrarenally formed AngII do not appear to directly constrict preglomerular vessels, including the afferent arterioles, when the RAS is activated physiologically. The sodium-retaining action of AngII may be due, in part, to constriction of efferent arterioles and to subsequent changes in peritubular capillary physical forces. However, AngII may also directly stimulate sodium reabsorption in proximal and distal tubules, although the exact site at which AngII increases distal tubular transport is still uncertain. Considerable evidence indicates that the direct intrarenal effects of AngII on tubular reabsorption, including those caused by changes in peritubular capillary physical forces or a direct action on tubular transport, are quantitatively more important than those mediated by changes in aldosterone secretion. Thus, the intrarenal effects of AngII provide a mechanism for stabilizing the GFR and excretion of metabolic waste products while causing sodium and water retention, thereby helping to regulate body fluid volumes and arterial pressure.