Peptide-Mediated Regulation of CSF Formation and Blood Flow to the Choroid Plexus

Author(s):  
Joanna Szmydynger-Chodobska ◽  
Adam Chodobski
Keyword(s):  
1989 ◽  
Vol 478 (1) ◽  
pp. 121-126 ◽  
Author(s):  
Frank M. Faraci ◽  
William G. Mayhan ◽  
Donald D. Heistad
Keyword(s):  

1983 ◽  
Vol 3 (3) ◽  
pp. 369-375 ◽  
Author(s):  
S. Nakamura ◽  
G. M. Hochwald

The effect of changes in brain blood flow on cerebrospinal fluid (CSF) volume flow rates, and that of changes in CSF volume flow rates on brain blood flow were determined in both normal and kaolin-induced hydrocephalic cats. In both groups of cats, blood flow in grey and white matter, cerebral cortex, and choroid plexus was measured with 105Ru microspheres during normocapnia, and again with 141Ce microspheres after arterial Pco2 was either increased by 300% or decreased by 50%. Blood flow measurements were also made during perfusion of the ventricular system with mock CSF and repeated during perfusion with anisosmotic mannitol solutions to alter CSF volume flow rate. In 30 normal and 26 hydrocephalic cats, blood flow to the cerebral cortex, white matter, and choroid plexus was similar; only blood flow to the caudate nucleus was greater in normal cats. The weight of the choroid plexus from hydrocephalic cats decreased by 17%. Blood flow in the choroid plexus of all cats decreased by almost 50% following hypercapnia or hypocapnia, without a change in the CSF volume flow rate. There was no change in cerebral or choroidal blood flow when CSF volume flow rate was either increased by 170% or decreased by 80%. These results suggest that choroid plexus blood flow does not limit or affect the volume flow rate of CSF from the choroid plexus. CSF volume flow rate can be altered without corresponding blood flow changes of the brain or choroid plexus. Choroid plexus blood flow and the reactivity of both brain and choroidal blood flow to changes in arterial Pco2 were not affected by the hydrocephalus. The lower CSF formation rate of hydrocephalic cats can be attributed in part to the decrease in the mass of choroid plexus tissue.


1991 ◽  
Vol 261 (5) ◽  
pp. R1126-R1132
Author(s):  
M. A. Maktabi ◽  
D. D. Heistad ◽  
F. M. Faraci

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)


2006 ◽  
Vol 14 (7S_Part_30) ◽  
pp. P1576-P1577 ◽  
Author(s):  
Li Zhao ◽  
Manuel Taso ◽  
Daniel Z. Press ◽  
David C. Alsop

1990 ◽  
Vol 258 (5) ◽  
pp. R1242-R1249
Author(s):  
R. B. Page ◽  
M. Gropper ◽  
E. Woodard ◽  
J. Townsend ◽  
S. Davis ◽  
...  

Blood flow was measured in the ovine median eminence and neural lobe before and after the intravenous infusion of dopamine (n = 7), the D1 agonist SKF 38393 (n = 4), the D2 agonist bromocriptine (n = 4), and the dopamine antagonist haloperidol (n = 5). It was also measured before and after the intracarotid infusion of dopamine into eight naive sheep and seven sheep pretreated with phenoxybenzamine. Radiolabeled microspheres were used to determine regional cerebral and regional neurohypophysial blood flows (RNHBF) in these 35 adult female sheep anesthetized with pentobarbital sodium. Samples for serum prolactin measurement by radioimmunoassay were obtained before and after drug infusion. Intravenous dopamine infusion did not change median eminence or neural lobe blood flow (RNHBF) but increased renal and choroid plexus blood flow. Intravenous haloperidol caused a significant fall in RNHBF and blood flow in choroid plexus, caudate nucleus, and kidneys. Intracarotid dopamine infusion decreased RNHBF but increased choroid plexus blood flow. RNHBF was significantly greater in the seven sheep pretreated with phenoxybenzamine than in the eight naive sheep. These findings do not support a role for dopamine in the regulation of median eminence blood flow. The last observation does add support to the hypothesis that norepinephrine or epinephrine interaction with alpha-receptors plays a role in the control of ovine median eminence blood flow and hence in the regulation of delivery of humoral messages from the brain to the anterior pituitary gland.


1959 ◽  
Vol 197 (4) ◽  
pp. 825-828 ◽  
Author(s):  
Edgar A. Bering

The cerebrospinal fluid production has been studied in the dog under conditions of maximum obtainable flow rates from the cisterna magna. Under these conditions the fluid had constant composition and was assumed to represent the cerebrospinal fluid in the intact state. Cerebral blood flow and cerebral oxygen consumption were measured by the method of Kety and Schmidt. The only significant correlations found were with oxygen consumption when the CSF flow rate was in terms of brain weight and with cerebral blood flow and cerebral vascular resistance when CSF flow was in terms of choroid plexus weight. A combined regression equation was calculated which satisfactorily accounted for the observed CSF flow: CSF cu mm/min. = .128 x CMRO2 x brain wgt. + 0.15 x CVR x choroid plexus wt. This suggested separate physiological processes, one correlated with oxygen metabolism and one with hydrodynamic factors of the cerebral blood flow. The data demonstrated that the choroid plexus alone could not have accounted for the entire CSF flow and some must have come from another source, presumably the brain.


1991 ◽  
Vol 260 (3) ◽  
pp. H902-H908 ◽  
Author(s):  
J. L. Williams ◽  
M. M. Thebert ◽  
K. A. Schalk ◽  
D. D. Heistad

The goal of this study was to examine effects of stimulation of the area postrema on blood flow to choroid plexus and brain. In chloralose-anesthetized dogs, the area postrema was stimulated electrically, and arterial pressure and blood gases were maintained at control levels. We measured blood flow to brain and choroid plexus of the fourth and lateral ventricles with microspheres. Stimulation of the area postrema at 10 +/- 2 microA (means +/- SE), which was the threshold for changes in arterial pressure and heart rate, decreased blood flow to choroid plexus of the fourth and lateral ventricles by 41 +/- 11 and 51 +/- 6%, respectively (from 349 +/- 38 and 503 +/- 46 ml.min-1.100 g-1, respectively). Stimulation at high amplitudes (67 +/- 5 microA) produced only slightly greater decreases in blood flow to choroid plexus. In contrast, cerebral blood flow did not change during stimulation of the area postrema. After blockade of autonomic ganglia with intravenous chlorisondamine, stimulation of the area postrema had minimal effects on blood flow to choroid plexus. The results indicate that stimulation of the area postrema decreases blood flow to choroid plexus, probably by an autonomic mechanism. We speculate that the area postrema may play a role in regulation of volume in the central nervous system by modulating production of cerebrospinal fluid.


1980 ◽  
Vol 197 (2) ◽  
pp. 532-537 ◽  
Author(s):  
Robert B. Page ◽  
David J. Funsch ◽  
Robert W. Brennan ◽  
Milton J. Herna´ndez
Keyword(s):  

Sign in / Sign up

Export Citation Format

Share Document