The Role of Angiotensin II in the Regulation of Blood Flow to Choroid Plexuses and Cerebrospinal Fluid Formation in the Rat

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Abstract
The effect of peripherally administered angiotensin II (AII) on blood flow to choroid plexuses was examined in pentobarbital-anesthetized rats. The indicator fractionation method with 123I- or 125I- N-isopropyl- p-iodoamphetamine as the marker was employed to measure blood flow. Basal blood flow to choroid plexus of the lateral cerebral ventricle (LVCP) (3.19 ± 0.23 ml g−1 min−1) was lower than that to choroid plexuses of the third (3VCP) and fourth (4VCP) ventricles (3.90 ± 0.38 and 3.95 ± 0.36 ml g−1 min−1, respectively). The effect of AII on choroidal blood flow varied depending on peptide dose and anatomical location of the choroidal tissue. AII infused intravenously at rates of 30 and 50 ng kg−1 min−1 decreased blood flow to both LVCP and 4VCP by 12–20%. Both lower (10 ng kg−1 min−1) and higher (100 and 300 ng kg−1 min−1) AII doses did not alter blood flow to LVCP and 4VCP. Blood flow to the 3VCP was not affected by any dose of the peptide used. In comparison, blood flow to cerebral cortex increased by 33% during intravenous AII infusion at a rate of 300 ng kg−1 min−1. The choroidal blood flow-lowering effect of moderate AII doses was abolished by both AT1 (losartan) and AT2 (PD 123319) receptor subtype antagonists (3 mg kg−1 i.v.). To determine whether the hemodynamic changes observed in choroid plexuses with moderate AII doses influence CSF formation, the ventriculocisternal perfusion was performed in rats (under the experimental conditions described) with Blue Dextran 2000 as the indicator. CSF production was not altered during intravenous infusion of AII at a rate of 30 ng kg−1 min−1. It is suggested that CSF formation is maintained in pathophysiological situations accompanied by increased plasma AII levels, which implicates a potential role for AII in regulating ion and water balance in the CNS.