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

1991 ◽  
Vol 71 (3) ◽  
pp. 795-800 ◽  
Author(s):  
S. Javaheri

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.

1991 ◽  
Vol 11 (5) ◽  
pp. 861-867 ◽  
Author(s):  
Christer Nilsson ◽  
Maria Lindvall-Axelsson ◽  
Christer Owman

Using laser-Doppler flowmetry during ventriculocisternal perfusion with inulin-[14C]carboxylic acid, choroid plexus blood flow (CPBF) and CSF production were measured simultaneously in rats during periods of 3 h. Blood flow and CSF production decreased only slightly during control experiments. The effect of vasoactive intestinal polypeptide (VIP) was studied at different concentrations of the peptide given either intraventricularly or intravenously. Intraventricular administration of VIP (10−9 or 10−7 M) resulted in a decrease in CSF production of up to 30%, while CPBF increased by 20%, also demonstrating that CSF production and blood flow are not directly coupled in the choroid plexus. When infused intravenously, VIP (10 or 100 pmol/kg/min) increased CPBF, an effect partly antagonized at higher concentrations owing to a VIP-induced systemic hypotension. No effect of VIP on CSF production could be seen with intravenous administration.


1990 ◽  
Vol 258 (1) ◽  
pp. R94-R98 ◽  
Author(s):  
F. M. Faraci ◽  
W. G. Mayhan ◽  
D. D. Heistad

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.


1979 ◽  
Vol 50 (5) ◽  
pp. 677-681 ◽  
Author(s):  
Steven K. Gudeman ◽  
Humbert G. Sullivan ◽  
Michael J. Rosner ◽  
Donald P. Becker

✓ 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.


Author(s):  
Arthur M. Feldman ◽  
Mel H. Epstein ◽  
Saul W. Brusilow

PEDIATRICS ◽  
1958 ◽  
Vol 22 (6) ◽  
pp. 1152-1152
Author(s):  
JONATHAN T. LANMAN

This Ciba Symposium records the proceedings of a meeting held in London in May, 1957 to discuss the cerebrospinal fluid. The papers presented may be roughly grouped in the fields of anatomy, physiology, and clinical medicine. Those in the field of anatomy are excellent and in keeping with the current renaissance in this field. They include observations on the early development of the telencephalic choroid plexus, suggesting a progression of diverse functions for this tissue during ontogeny, and a study of the mature choroid plexus using the electron microscope.


Science ◽  
1971 ◽  
Vol 173 (3994) ◽  
pp. 330-332 ◽  
Author(s):  
T. H. Milhorat ◽  
M. K. Hammock ◽  
J. D. Fenstermacher ◽  
D. P. Rall ◽  
V. A. Levin

1998 ◽  
Vol 275 (2) ◽  
pp. F235-F238 ◽  
Author(s):  
Adam Chodobski ◽  
Joanna Szmydynger-Chodobska ◽  
Michael J. McKinley

Cerebrospinal fluid (CSF) plays an important role in the brain’s adaptive response to acute osmotic disturbances. In the present experiments, the effect of 48-h dehydration on CSF formation and absorption rates was studied in conscious adult sheep. Animals had cannulas chronically implanted into the lateral cerebral ventricles and cisterna magna to enable the ventriculocisternal perfusion. A 48-h water deprivation altered neither CSF production nor resistance to CSF absorption. However, in the water-depleted sheep, intraventricular pressure tended to be lower than that found under control conditions. This likely resulted from decreased extracellular fluid volume and a subsequent drop in central venous pressure occurring in dehydrated animals. In conclusion, our findings provide evidence for the maintenance of CSF production during mild dehydration, which may play a role in the regulation of fluid balance in the brain during chronic hyperosmotic stress.


Science ◽  
1978 ◽  
Vol 201 (4351) ◽  
pp. 176-178 ◽  
Author(s):  
M Lindvall ◽  
L Edvinsson ◽  
C Owman

2004 ◽  
Vol 40 (6) ◽  
pp. 277-283 ◽  
Author(s):  
P.L. Longatti ◽  
L. Basaldella ◽  
E. Orvieto ◽  
A. Fiorindi ◽  
A. Carteri

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