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 Humoral regulation of blood flow to choroid plexus: role of arginine vasopressin.

1988 ◽  
Vol 63 (2) ◽  
pp. 373-379 ◽  
Author(s):  
F M Faraci ◽  
W G Mayhan ◽  
W J Farrell ◽  
D D Heistad
Keyword(s):  
Blood Flow ◽  
Choroid Plexus ◽  
Arginine Vasopressin ◽  
Humoral Regulation

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.

scholarly journals Effect of Atriopeptin on Production of Cerebrospinal Fluid

1992 ◽  
Vol 12 (4) ◽  
pp. 691-696 ◽  
Author(s):  
Kimberly A. Schalk ◽  
Frank M. Faraci ◽  
John L. Williams ◽  
Dianna VanOrden ◽  
Donald D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Intravenous Infusion ◽  
Intracerebroventricular Injection ◽  
Increase Blood Flow ◽  
Small Decrease ◽  
Cerebral Ventricles ◽  
Ventriculocisternal Perfusion ◽  
Increased Blood Flow

We reported previously that intravenous infusion of atriopeptin increases blood flow to the choroid plexus. The first goal of this study was to determine whether blood-borne atriopeptin increases the production of CSF. Ventriculocisternal perfusion was used to measure the production of CSF in anesthetized rabbits. Atriopeptin increased blood flow to the choroid plexus (measured with microspheres) but did not alter the production of CSF. The second goal of the study was to determine whether intracerebroventricular injection of atriopeptin affects the production of CSF. Injection of atriopeptin into the cerebral ventricles increased blood flow to the choroid plexus but produced a small decrease in production of CSF. In summary, blood-borne and intraventricular atriopeptin increase blood flow to the choroid plexus, but do not increase the production of CSF.

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.

Changes in cerebral blood flow and oxygen metabolism during moderate hypothermia in patients with severe middle cerebral artery infarction

2000 ◽  
Vol 8 (5) ◽  
pp. 1-4 ◽  
Author(s):  
Emanuela Keller ◽  
Thorsten Steiner ◽  
Javier Fandino ◽  
Stefan Schwab ◽  
Werner Hacke
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Mild Hypothermia ◽  
Indicator Dilution ◽  
Dilution Method ◽  
Moderate Hypothermia ◽  
Double Indicator Dilution

Object Moderate hypothermia has been reported to be effective in the treatment of postischemic brain edema. The effect of hypothermia on cerebral hemodynamics is a matter of controversial discussion in literature. Clinical studies have yet to be performed in patients with ischemic stroke after induction of hypothermia. Methods Measurements during mild hypothermia (33–34°C) were made in six patients with severe ischemic stroke involving the middle cerebral artery territory. Hypothermia was induced as soon as possible and maintained for 48 to 72 hours. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were estimated by a new double-indicator dilution method. Measurements of CBF were made during normothermia, immediately after induction of hypothermia, at the end of hypothermia, and after rewarming. A total of 19 measurements of CBF and jugular bulb O2 saturation were made. Immediately after induction of hypothermia, CBF decreased in all patients. During late hypothermia, CBF improved in patients who survived but remained diminished in the two patients who died. Reduced CMRO2 levels were observed during all phases of hypothermia in all but one case. Conclusions Preliminary oberservations indicate that moderate hypothermia seems to reduce CMRO2 Immediately after induction of hypothermia, CBF may decrease in all patients. During late hypothermia CBF seems to recover in patients with good outcome but remains diminished in patients who die. Serial bedside CBF measurements with the new double-indicator dilution technique may be useful to describe cerebral hemodynamic characteristics in patients with severe ischemic stroke during hypothermia.

Cerebrospinal fluid formation and absorption in dehydrated sheep

1998 ◽  
Vol 275 (2) ◽  
pp. F235-F238 ◽  
Author(s):  
Adam Chodobski ◽  
Joanna Szmydynger-Chodobska ◽  
Michael J. McKinley
Keyword(s):  
Cerebrospinal Fluid ◽  
Adaptive Response ◽  
Venous Pressure ◽  
Extracellular Fluid ◽  
Cerebral Ventricles ◽  
Central Venous ◽  
Ventriculocisternal Perfusion ◽  
Fluid Formation ◽  
The Brain ◽  
Csf Production

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.

scholarly journals Effects of Arterial Pco2 and Cerebrospinal Fluid Volume Flow Rate Changes on Choroid Plexus and Cerebral Blood Flow in Normal and Experimental Hydrocephalic Cats

1983 ◽  
Vol 3 (3) ◽  
pp. 369-375 ◽  
Author(s):  
S. Nakamura ◽  
G. M. Hochwald
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Cortex ◽  
Choroid Plexus ◽  
Flow Rate ◽  
Volume Flow Rate ◽  
Volume Flow ◽  
Brain Blood Flow ◽  
Choroidal Blood Flow ◽  
Flow Rates

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.

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.

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