Effect of acetazolamide and furosemide on the production and composition of cerebrospinal fluid from the cat choroid plexus

1982 ◽  
Vol 60 (3) ◽  
pp. 405-409 ◽  
Author(s):  
James M. Melby ◽  
Lewis C. Miner ◽  
Donal J. Reed
Keyword(s):  
Cerebrospinal Fluid ◽  
Drug Treatment ◽  
Choroid Plexus ◽  
Transport Mechanism ◽  
Electrolyte Composition ◽  
K Concentration ◽  
Drug Free ◽  
K Transport ◽  
Csf Production

The effect of acetazolamide and furosemide on choroid plexus (CP) production and electrolyte composition of cerebrospinal fluid (CSF) from the cat CP in situ was investigated. Both drugs decreased CSF production by the CP by 50–90% from a control rate of 0.53 μL ∙ min−1 ∙ mg−1 CP within 1.5–2.5 h after the start of drug treatment. The results were similar whether the drug was administered intravenously or applied directly to the CSF side of the CP. A number of experiments in which the effect of administering drugs via the chamber were studied were continued with the drugs removed by washing the preparation with drug-free artificial CSF and the responses measured. The results demonstrated that the effects of acetazolamide and furosemide were reversed during the 1st h following the washout. Both drugs decreased K concentration of nascent CSF when administered intravenously and furosemide also did so when administered on the CSF side of the CP. It is concluded from these and previous data that acetazolamide and furosemide markedly inhibit the transport mechanism(s) in the cat CP that are responsible for CP secretion which represents about 40–60% of the total CSF production and that K transport is also affected.

Surgical removal of bilateral papillomas of the choroid plexus of the lateral ventricles with resolution of hydrocephalus

1979 ◽  
Vol 50 (5) ◽  
pp. 677-681 ◽  
Author(s):  
Steven K. Gudeman ◽  
Humbert G. Sullivan ◽  
Michael J. Rosner ◽  
Donald P. Becker
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Large Volume ◽  
Surgical Removal ◽  
Tumor Removal ◽  
Content Type ◽  
Lateral Ventricles ◽  
Csf Diversion ◽  
Csf Production ◽  
Fine Print

✓ The authors report a patient with bilateral papillomas of the choroid plexus of the lateral ventricles with documentation of cerebrospinal fluid (CSF) hypersecretion causing hydrocephalus. Special attention is given to the large volume of CSF produced by these tumors (removal of one tumor reduced CSF outflow by one-half) and to the fact that CSF diversion was not required after both tumors were removed. Since tumor removal alone was sufficient to stop the progression of hydrocephalus, we feel that this case supports the concept that elevated CSF production by itself is sufficient to cause hydrocephalus in patients with papillomas of the choroid plexus.

scholarly journals Cerebrospinal fluid formation is controlled by membrane transporters to modulate intracranial pressure

2021 ◽  
Author(s):  
Eva K. Oernbo ◽  
Annette B. Steffensen ◽  
Pooya Razzaghi Khamesi ◽  
Trine L. Toft-Bertelsen ◽  
Dagne Barbuskaite ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Choroid Plexus ◽  
Molecular Mechanisms ◽  
Osmotic Gradient ◽  
Pharmaceutical Therapy ◽  
Osmotic Water ◽  
Life Threatening ◽  
Molecular Mode ◽  
Csf Production

AbstractDisturbances in the brain fluid balance can lead to life-threatening elevation in the intracranial pressure (ICP), which represents a vast clinical challenge. Nevertheless, the molecular mechanisms governing cerebrospinal fluid (CSF) secretion are largely unresolved, thus preventing targeted and efficient pharmaceutical therapy of cerebral pathologies involving elevated ICP. Here, we employed experimental rats to demonstrate low osmotic water permeability of the choroid plexus, lack of an osmotic gradient across this tissue, and robust CSF secretion against osmotic gradients. Together, these results illustrate that CSF secretion occurs independently of conventional osmosis, which challenges the existing assumption that CSF production is driven entirely by bulk osmotic forces across the CSF-secreting choroid plexus. Instead, we reveal that the choroidal Na+/K+/Cl− cotransporter NKCC1, Na+/HCO3− cotransporter NBCe2, and Na+/K+-ATPase are actively involved in CSF production and propose a molecular mode of water transport supporting CSF production in this secretory tissue. Further, we demonstrate that inhibition of NKCC1 directly reduces the ICP, illustrating that altered CSF secretion may be employed as a strategy to modulate ICP. These insights identify new promising therapeutic targets against brain pathologies associated with elevated ICP.

Role of NaCl cotransport in cerebrospinal fluid production: effects of loop diuretics

1991 ◽  
Vol 71 (3) ◽  
pp. 795-800 ◽  
Author(s):  
S. Javaheri
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Ionic Composition ◽  
Reasonable Assumption ◽  
Cerebral Ventricles ◽  
Fluid Production ◽  
Production Effects ◽  
Nacl Cotransport ◽  
Csf Production

Cerebrospinal fluid (CSF) is secreted primarily by the choroid plexus (CP) located in the cerebral ventricles. Although much is known about ionic composition of cisternal CSF, the mechanisms involved in secretion of CSF in mammals are still not understood. The main aim of this report is to critically review the role of NaCl cotransport carrier in CSF production. On the basis of the studies in the literature, a model for CSF production by the CP is proposed. In this model, CP cells are assumed to be equipped with an NaCl cotransport carrier located on the basolateral (blood-facing) membrane. Because Na+ and Cl- are the two principal ions in CSF, their continued secretions into cerebral ventricles by CP cells require an adequate intracellular supply, which may be guaranteed by the NaCl cotransport carrier. Although this appears to be a reasonable assumption, making the processes involved in CSF production similar to those of other secretory epithelial cells, the presence of such a carrier in mammalian CP remains controversial. The reasons for this controversy are critically reviewed, and some suggestions for further studies are made.

Active transport of chloride by lateral ventricle choroid plexus of the rat

1985 ◽  
Vol 249 (4) ◽  
pp. F470-F477 ◽  
Author(s):  
Q. R. Smith ◽  
C. E. Johanson
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Active Transport ◽  
Lateral Ventricle ◽  
Bath Temperature ◽  
Methyl Sulfate ◽  
Choroid Plexus Epithelium ◽  
Adult Rat ◽  
Cation Substitutions ◽  
K Transport

The nature of Cl transport and its relation to Na and K transport were analyzed in adult rat lateral ventricle choroid plexus incubated in cerebrospinal fluid (CSF) medium at 37 degrees C and PCO2 = 30 mmHg. In synthetic CSF (extracellular Cl [( Cl]o) = 130 mM), the intracellular Cl [( Cl]i) was three times that estimated for passive distribution. Choroid plexus [Cl]i was not determined by Donnan distribution because [Cl]i remained constant at approximately 50 mM while the [K]i/[K]o ratio was varied 10-fold by drugs and cation substitutions. A [Cl]i/[Cl]o ratio of approximately 0.38 was found when [Cl]o was varied from 15 to 130 mM by isosmotic replacement of Cl with methyl sulfate or isethionate. However, the [Cl]i/[Cl]o ratio increased to greater than 1.0 when [Cl]o was lowered below 5 mM. Reduction in bath temperature to 15 degrees C (CSF PCO2 = 50 mmHg) increased both [Cl]i/[Cl]o and [HCO3]i/[HCO3]o to approximately 0.6. SITS, an inhibitor of Cl-HCO3 transport, reduced [Cl]i by 18 mM, decreasing the [Cl]i/[Cl]o ratio close to the equilibrium value. In contrast, neither furosemide (10(-3) M) nor low CSF [Na]o (3 mM) reduced Cl accumulation. It is concluded that uphill movement of Cl into choroid plexus epithelium occurs primarily by Cl-HCO3 antiport and not by Na-Cl symport.

scholarly journals The Wilms Tumor Gene wt1a Contributes to Blood-Cerebrospinal Fluid Barrier Function in Zebrafish

2022 ◽  
Vol 9 ◽  
Author(s):  
Vera L. Hopfenmüller ◽  
Birgit Perner ◽  
Hanna Reuter ◽  
Thomas J. D. Bates ◽  
Andreas Große ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Wilms Tumor ◽  
Barrier Properties ◽  
Suppressor Gene ◽  
Ependymal Cells ◽  
Urogenital Development ◽  
And Function ◽  
Dorsal Hindbrain

The Wilms tumor suppressor gene Wt1 encodes a zinc finger transcription factor, which is highly conserved among vertebrates. It is a key regulator of urogenital development and homeostasis but also plays a role in other organs including the spleen and the heart. More recently additional functions for Wt1 in the mammalian central nervous system have been described. In contrast to mammals, bony fish possess two paralogous Wt1 genes, namely wt1a and wt1b. By performing detailed in situ hybridization analyses during zebrafish development, we discovered new expression domains for wt1a in the dorsal hindbrain, the caudal medulla and the spinal cord. Marker analysis identified wt1a expressing cells of the dorsal hindbrain as ependymal cells of the choroid plexus in the myelencephalic ventricle. The choroid plexus acts as a blood-cerebrospinal fluid barrier and thus is crucial for brain homeostasis. By employing wt1a mutant larvae and a dye accumulation assay with fluorescent tracers we demonstrate that Wt1a is required for proper choroid plexus formation and function. Thus, Wt1a contributes to the barrier properties of the choroid plexus in zebrafish, revealing an unexpected role for Wt1 in the zebrafish brain.

scholarly journals Transfer of Magnesium across the Perfused Choroid Plexus of Sheep

1986 ◽  
Vol 39 (2) ◽  
pp. 161 ◽  
Author(s):  
TF Allsop
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Electrolyte Composition ◽  
Perfusion Fluid ◽  
Transfer Rates ◽  
Sheep Blood ◽  
Low Concentrations

Isolated perfused choroid plexus preparations from sheep were used to study the effects of low concentrations of magnesium in the perfusion fluid on the transfer of magnesium into choroid plexus fluid (CPF). A perfusion fluid of similar electrolyte composition to sheep blood resulted in CPF similar to ventricular cerebrospinal fluid at a rate of 2�2 III min - 1 mg -I dry choroidal tissue. Decreasing the concentration of magnesium in the perfusion fluid caused a fall in the concentration of magnesium in the CPF, although it remained higher than in the perfusion fluid. The rate of transfer of magnesium from the perfusion fluid to the CPF decreased in the presence of high levels of potassium in the perfusion fluid. But decreasing the concentration of calcium in the perfusion fluid had no effect on magnesium transfer rates.

Hydrocephalus secondary to diffuse villous hyperplasia of the choroid plexus

1996 ◽  
Vol 85 (4) ◽  
pp. 689-691 ◽  
Author(s):  
Gavin W. Britz ◽  
D. Kyle Kim ◽  
John D. Loeser
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Resonance Imaging ◽  
Ventriculoatrial Shunt ◽  
Content Type ◽  
Tomography Scanning ◽  
Csf Production ◽  
Choroid Plexus Papillomas ◽  
Fine Print

✓ Diffuse villous hyperplasia of the choroid plexus, which is distinct from bilateral choroid plexus papillomas, is extremely rare and is often associated with hydrocephalus due to the overproduction of cerebrospinal fluid (CSF). The authors describe an infant with hydrocephalus, diagnosed by computerized tomography scanning, who developed ascites following placement of a ventriculoperitoneal shunt and, subsequently, demonstrated excessive CSF production when the shunt was externalized. The patient was later successfully treated by placement of a ventriculoatrial shunt. Magnetic resonance imaging demonstrated diffuse villous hyperplasia of the choroid plexus as the cause of the patient's hydrocephalus. The literature on diffuse villous hyperplasia of the choroid plexus is reviewed.

Rubidium entry into brain and cerebrospinal fluid during acute and chronic alterations in plasma potassium

1994 ◽  
Vol 266 (6) ◽  
pp. H2239-H2246
Author(s):  
W. Stummer ◽  
R. F. Keep ◽  
A. L. Betz
Keyword(s):  
Cerebrospinal Fluid ◽  
Brain Tissue ◽  
Blood Brain Barrier ◽  
Plasma Potassium ◽  
K Uptake ◽  
Passive Permeability ◽  
Permeability Surface ◽  
K Concentration ◽  
Acute Changes ◽  
K Transport

To elucidate whether K+ uptake across the blood-brain barrier (BBB) or blood-cerebrospinal fluid (CSF) barrier is subject to acute or chronic regulation, rats were rendered acutely or chronically hyper- or hypokalemic (range: 2.8–7.2 mM). Measurements were made of the permeability-surface (PS) products of 86Rb+, a marker for K+, and alpha-[3H]aminoisobutyric acid (AIB), a passive permeability marker, and of CSF K+ concentration ([K+]CSF). [K+]CSF decreased by 8% in chronic hypokalemia P < 0.01), but otherwise remained unchanged. The AIB PS products were unaltered in any group, excluding a change in passive permeability. The Rb PS product, however, increased by 31% for brain tissue (P < 0.01) and by 46% for CSF (P < 0.05) during acute hypokalemia, but was unchanged during acute hyperkalemia. During chronic hypokalemia the Rb PS product increased by 40% for brain (P < 0.01) and 55% for CSF (P < 0.01) and decreased during chronic hyperkalemia by 37% for brain (P < 0.01) and 49% (P < 0.01) for CSF. Unidirectional K+ fluxes were calculated, revealing greater regulation of K+ influx into both brain tissue and CSF during chronic compared with acute changes of plasma K+ concentration ([K+]pl). Our results suggest that K+ transport is saturable at both the BBB and the blood-CSF barriers under normal conditions and that both barriers adapt to chronic changes in [K+]pl by modifying specific, transcellular routes of K+ entry.

Effect of vasopressin on production of cerebrospinal fluid: possible role of vasopressin (V1)-receptors

1990 ◽  
Vol 258 (1) ◽  
pp. R94-R98 ◽  
Author(s):  
F. M. Faraci ◽  
W. G. Mayhan ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Arginine Vasopressin ◽  
Indicator Dilution ◽  
Dilution Method ◽  
Ventriculocisternal Perfusion ◽  
Csf Production ◽  
Humoral Regulation

The goal of this study was to examine the role of arginine vasopressin in humoral regulation of choroid plexus function. Production of cerebrospinal fluid (CSF) was measured in anesthetized rabbits with an indicator dilution method, by using ventriculocisternal perfusion of artificial CSF containing blue dextran. Rabbits received either vehicle, vasopressin or vasopressin in the presence of the V1-antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]arginine vasopressin ([d(CH2)5Tyr(Me)]-AVP). Under control conditions, blood flow to the choroid plexus (measured with microspheres) averaged 369 +/- 26 (mean +/- SE) ml.min-1.100 g-1 and CSF production averaged 9.9 +/- 0.9 microliters/min. Intravenous infusion of vasopressin (2 mU.kg-1.min-1 for 90 min) decreased blood flow to the choroid plexus by 50-60% for the entire period of infusion. Vasopressin decreased production of CSF by 35 +/- 8%. Blood flow to the choroid plexus and production of CSF did not change significantly from control values in animals that received vehicle. In the presence of the V1-antagonist (10 micrograms/kg), infusion of vasopressin had no effect on blood flow to the choroid plexus or production of CSF. Thus circulating vasopressin, at plasma levels that are observed under physiological and pathophysiological conditions, has important effects on formation of CSF, as well as on blood flow to the choroid plexus. These findings are consistent with the hypothesis that effects of vasopressin on both variables are mediated through vasopressin (V1)-receptors.

scholarly journals Autonomic Nerves in the Mammalian Choroid Plexus and Their Influence on the Formation of Cerebrospinal Fluid

1981 ◽  
Vol 1 (3) ◽  
pp. 245-266 ◽  
Author(s):  
Maria Lindvall ◽  
Christer Owman
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Sympathetic Nerves ◽  
Inhibitory Effect ◽  
Cholinergic Innervation ◽  
Autonomic Nerves ◽  
Pronounced Increase ◽  
Csf Production ◽  
Stimulation Of

The choroid plexuses of all ventricles receive a well-developed adrenergic and cholinergic innervation reaching both the secretory epithelium and the vascular smooth muscle cells. Also peptidergic nerves, containing vasoactive intestinal polypeptide, are present but primarily associated only with the vascular bed. A sympathetic inhibitory effect on the plexus epithelium has been indicated in determinations of carbonic anhydrase activity and by studies of various aspects of active transport in isolated plexus tissue. Pharmacological analysis in vitro has shown the choroidal arteries to possess both vasoconstrictory α-adrenergic and vasodilatory β-adrenergic receptors. Electrical stimulation of the sympathetic nerves, which originate in the superior cervical ganglia, induces as much as 30% reduction in the net rate of cerebrospinal fluid (CSF) production, while sympathectomy results in a pronounced increase, about 30% above control, in the CSF formation. There is strong reason to believe that the choroid plexus is under the influence of a considerable sympathetic inhibitory tone under steady-state conditions. From pharmacological and biochemical experiments it is suggested that the sympathomimetic reduction in the rate of CSF formation is the result of a combined β-receptormediated inhibition of the secretion from the plexus epithelium and a reduced blood flow in the choroid plexus tissue resulting from stimulation of the vascular α-receptors. The choroid plexus probably also represents an important inactivation site and gate mechanism for sympathomimetic amines, as evidenced by considerable local activity of catechol- O-methyl transferase and monoamine oxidase, primarily type B. The CSF production rate is also reduced by cholinomimetic agents, suggesting the presence of muscarinic-type cholinergic receptors in the choroid plexus.

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