Maktabi M A, Stachovic G C, Faraci F M
Department of Anesthesia, University of Iowa College of Medicine, Iowa City 52242.
Brain Res. 1993 Mar 19;606(1):44-9. doi: 10.1016/0006-8993(93)91567-c.
The choroid plexus, which produces cerebrospinal fluid (CSF), contains receptors for angiotensin II and a very high concentration of angiotensin-converting enzyme. Circulating angiotensin II decreases blood flow to the choroid plexus. The first goal of this study was to examine the hypothesis that angiotensin II decreases the production of CSF. The second goal was to determine whether effects of angiotensin II on the production of CSF were receptor-mediated. Production of CSF was measured in chloralose-anesthetized rabbits using ventriculocisternal perfusion of artificial CSF containing blue dextran. Rabbits received either vehicle, angiotensin II, angiotensin II in the presence of an angiotensin II antagonist (saralasin), or saralasin intravenously. Increases in blood pressure, during administration of angiotensin II, were prevented by withdrawal of blood. Under control conditions, CSF production averaged 7.2 +/- 0.2 microliters/min (mean +/- S.E.). Angiotensin II (100 ng/kg/min i.v.) decreased CSF production by 24 +/- 3% (P < 0.05, n = 8). In the presence of saralasin (1 microgram/kg/min i.v.), angiotensin II had no significant effect on CSF production (-4 +/- 6%, P > 0.05, n = 7). Vehicle did not affect CSF production significantly (-2 +/- 6%, P > 0.05, n = 7). Saralasin alone decreased production of CSF (-21 +/- 5%, P < 0.05, n = 7). To test the specificity of saralasin in blocking effects of angiotensin II receptor stimulation on CSF production, the carbonic anhydrase inhibitor acetazolamide was administered in the presence and absence of saralasin.(ABSTRACT TRUNCATED AT 250 WORDS)
