Effects of central and intravascular angiotensin I and II on the choroid plexus.

The choroid plexus contains receptors for angiotensin II (ANG II) and a very high concentration of angiotensin-converting enzyme. The goal of this study was to test the hypothesis that central, as well as circulating, ANG I and II decrease blood flow to the choroid plexus. Under control conditions in anesthetized rabbits, blood flow (microspheres) to the choroid plexus was 449 +/- 21 (mean +/- SE) ml.min-1.100 g(-1). Intravascular ANG I (30 and 100 ng.kg-1.min-1) decreased blood flow to the choroid plexus by 19 +/- 14 and 28 +/- 18%, respectively. Intravascular ANG II (30 and 100 ng.kg-1.min-1) also produced a decrease in blood flow by 28 +/- 9 and 47 +/- 7%, respectively. When administered into the lateral ventricle, ANG I and II (10 and 100 ng.kg-1.min-1) decreased blood flow to a similar degree: 22 +/- 11 and 31 +/- 10% and 12 +/- 10 and 27 +/- 8%, respectively. Cerebral blood flow was not decreased by intravascular or central ANG I or II. The angiotensin-converting enzyme inhibitor quinaprilat prevented the decrease in blood flow to the choroid plexus in response to ANG I without affecting responses to ANG II. Thus 1) circulating ANG I and II are potent constrictors of blood vessels of the choroid plexus, 2) the constrictor effect of ANG I on the blood vessels of the choroid plexus appears mediated primarily by generation of ANG II, and 3) intracerebroventricular ANG I produces large reductions in the blood flow to the choroid plexus, which suggests that there is an effective central system that converts ANG I to ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)