The existence of the brain-renin angiotensin system has been the subject of several reviews (36, 37, 86, 93). All the components of the renin-angiotensin cascade have been described in the brain, although their exact interaction is not yet defined. Angiotensin (Ang) II in brain has been quantified and characterized by high-pressure liquid chromatography (HPLC)(46, 73, 91, 97). The levels are in the picogram range, but a concentration of 1 picogram of Ang II per gram brain tissue is 1000-3000 times greater than that of 1 picogram per milliliter found in plasma, because brain tissue contains 1-3 ILl plasma per gram.

This review attempts to summarize the emerging picture of the physiolo gical functions and significance of brain Ang II. Several diverse effects have been reported for Ang II in the brain. Some of these effects can be achieved with peripherally administered doses, but others occur only with in traventricular (ivt) or direct microinjections into the brain. A brief survey of the effects of central versus peripheral angiotensin indicates that there are substantial differences between these two sources of the hormone (Table 1). Some of these differences in effect are a matter of degree. For example, the dose required to induce thirst depends on whether Ang II is administered centrally or peripherally, but this may also reflect different mechanisms. It is hard to assess the actual dose equivalency between blood-borne angiotensin and angiotensin injected directly into the brain because the availability of, and the access to, receptors differ. Direct injection into the brain allows an giotensin to reach many receptor sites. Systemic infusion of Ang II, however, can only reach sites in the brain that have no blood-brain barrier (BBB); these