Uptake of [<sup>14</sup>C]urea by the <i>in vivo</i> choroid plexus—cerebrospinal fluid—brain system: identification of sites of molecular sieving

Johanson, Conrad E.; Woodbury, Dixon M.

doi:10.1113/jphysiol.1978.sp012183

Cited by 40 publications

(28 citation statements)

References 21 publications

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“…Moreover, the present observation that the 14C-urea space in the CP does not change after long-term nephrectomy indicates that the permeability of the basolateral mem brane in the plexus to urea (i.e., the blood-CSF barrier; see ref. 16) is not modified in uremia.…”

Section: Permeability O F the Blood-brain And Blood-csf Barriersmentioning

confidence: 99%

“…In the calculation of cellular |Na| and | K. ] for cerebral cortex, CSF electrolyte concentrations were used. Radioisotope spaces were calculated by con ventional formulae (16). increased substantially from 4.3 in controls to 11.6 mmol/1 in the 48-hour animals (p <0.01).…”

Section: Calculationsmentioning

confidence: 99%

“…Finally, a piece of skeletal muscle was sampled, cleaned and weighed. Tissues and fluids were analyzed for radioisotopes and electrolytes by methods pre viously described (14,16).…”

Section: Tissue Sampling and Analysismentioning

confidence: 99%

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The Sink Action of Cerebrospinal Fluid in Uremia

Hise¹,

Johanson²

1979

Eur Neurol

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The distribution of water, electrolytes and non-electrolytes in various compartments of the central nervous system was analyzed in rats subjected to various stages of uremia. After bilateral nephrectomy for various periods of time ranging from 1 to 48 h, there is a progressive hyperkalemia, hyponatremia and metabolic acidosis. Although the cerebrospinal fluid (CSF) [K] progressively increases to a concentration of 6 mmol/l at 48 h post-nephrectomy, the ratio of CSF [K]/plasma [K] remains relatively constant throughout the duration of the uremic challenge; on the other hand, the concentration gradient for Na (CSF to plasma) markedly increases with progression of uremia. The steady rise in cellular [K] in both the choroid plexus and in at least one compartment of the cerebral cortex is presumably a reflection of stimulation of the Na-K pump caused by a build-up in [K] in the extracellular fluids of the brain. The blood-brain and blood-CSF barrier systems to both ¹⁴C-urea and ¹³¹I remain intact 24–48 h after nephrectomy; and there is not any evidence of cerebral edema at any stage of uremia. Thus, several lines of evidence indicate that the CSF-sink effect is maintained even in advanced uremia.

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Section: Permeability O F the Blood-brain And Blood-csf Barriersmentioning

confidence: 99%

Section: Calculationsmentioning

confidence: 99%

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The Sink Action of Cerebrospinal Fluid in Uremia

Hise¹,

Johanson²

1979

Eur Neurol

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“…Reconstructed from micrographs, this schematic portrays three major compartments of the CP: an inner vascular core (20% of tissue volume), the intermediate interstitial zone containing a loose stroma and interstitial fluid (ISF) zone (15% of tissue volume), and an outer circumferential ring of epithelial cells (65% of tissue volume). Solutes in blood readily diffuse out of CP capillaries into and through the ISF up to the epithelial basal membrane, which restricts diffusion (Johanson and Woodbury 1978). To cross the blood-cerebrospinal fluid barrier (BCSFB), a substance must be actively transported across the epithelium (transcellular route) and/or diffuse passively between cells (paracellular route).…”

Section: Toxico-pathologic Considerations For Choroid Plexuscerebrospmentioning

confidence: 99%

The Distributional Nexus of Choroid Plexus to Cerebrospinal Fluid, Ependyma and Brain

et al. 2010

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Bordering the ventricular cerebrospinal fluid (CSF) are epithelial cells of choroid plexus (CP), ependyma and circumventricular organs (CVOs) that contain homeostatic transporters for mediating secretion/reabsorption. The distributional pathway (''nexus'') of CP-CSF-ependyma-brain furnishes peptides, hormones, and micronutrients to periventricular regions. In disease/toxicity, this nexus becomes a conduit for infectious and xenobiotic agents. The sleeping sickness trypanosome (a protozoan) disrupts CP and downstream CSF-brain. Piperamide is anti-trypanosomic but distorts CP epithelial ultrastructure by engendering hydropic vacuoles; this reflects phospholipidosis and altered lysosomal metabolism. CP swelling by vacuolation may occlude CSF flow. Toxic drug tools delineate injuries to choroidal compartments: cyclophosphamide (vasculature), methylcellulose (interstitium), and piperazine (epithelium). Structurally perturbed CP allows solutes to penetrate the ventricles. There, CSF-borne pathogens and xenobiotics may permeate the ependyma to harm neurogenic stem cell niches. Amoscanate, an anti-helmintic, potently injures rodent ependyma. Ependymal/brain regions near CP are vulnerable to CSF-borne toxicants; this proximity factor links regional barrier breakdown to nearby periventricular pathology. Diverse diseases (e.g., African sleeping sickness, multiple sclerosis) take early root in choroidal, circumventricular, or perivascular loci. Toxicokinetics informs on pathogen, anti-parasitic agent, and auto-antibody distribution along the CSF nexus. CVOs are susceptible to plasma-borne toxicants/pathogens. Countering the physico-chemical and pathogenic insults to the homeostasis-mediating ventricle-bordering cells sustains brain health and fluid balance.

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“…Mannitol (mol wt 180), a sugar alcohol with relatively low permeativity in brain, has been used as an extra cellular marker in peripheral tissues and choroid plexus (Johanson, 1980;Smith et a\., 1981). Urea (mol wt 60), also nonionized, rapidly enters cells in the periphery but enters eNS slowly (t'/2 = 1-2 h) (Johanson and Woodbury, 1978). Since these tracer molecules penetrate eNS at widely different rates under control conditions (Parandoosh and Jo hanson, 1982;Smith et aI., 1982), we considered it useful to analyze the effects of sympathomimetic agents on the relative and absolute volumes of distribution (Vd) of these compounds in hypo-, normo-, and hypertensive animals, to explore fur ther the mechanisms of permeability disruption of eNS barrier systems.…”

mentioning

confidence: 99%

Adrenergic-Induced Enhancement of Brain Barrier System Permeability to Small Nonelectrolytes: Choroid Plexus versus Cerebral Capillaries

Murphy

Johanson

1985

J Cereb Blood Flow Metab

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Summary: Acute hypertension induced by adrenergic agents opens up the blood-CSF barrier (choroid plexus) to nonelectrolyte and protein tracers. Sprague-Dawley adult rats anesthetized with ketamine were given an in travenous bolus of either epinephrine (10 f,Lg/kg), phen ylephrine (100 f,Lg/kg), isoproterenol (10 f,Lg/kg), or D,L amphetamine (2 mg/kg). Tr acers were injected simulta neously with test agents, and the animals killed 10 min later. Epinephrine raised MABP by 57 mm Hg, to a peak pressure of 160 mm Hg; and it increased the volume of distribution (Vd) of urea, mannitol, and 125I-bovine serum albumin in CSF by l.5-, 2.7-, and 30-fold, respectively.There was enhanced uptake by lateral and fourth ven tricle choroid plexuses, cerebral cortex, cerebellum, me dulla, and thalamus. Phenylephrine also elevated MABP to 160 mm Hg, but it increased permeation of tracers into CSF (and several brain regions) to a lesser extent than Adrenergic agonists that raise blood pressure can open the blood-brain barrier (BBB) to large mole cules such as albumin and horseradish peroxidase and to smaller molecules like inulin and norepi nephrine (Johansson, 1980). Metaraminol, epineph rine, amphetamine, norepinephrine, and phenyl ephrine increase BBB permeability, but if the agent induced rise in blood pressure is blocked, no change in tracer permeation is observed (Johansson, 1980). A rise in intracarotid pressure concurrent with sys temic hypervolemia also opens the BBB (Nagy et aI., 1979). Augmented penetration of isotopes with adrenergic agonists is related to the rate and extent of blood pressure rise and to the size of the cerebral vessel lumen; vasoconstriction generally decreases

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Uptake of [¹⁴C]urea by the in vivo choroid plexus—cerebrospinal fluid—brain system: identification of sites of molecular sieving

Cited by 40 publications

References 21 publications

The Sink Action of Cerebrospinal Fluid in Uremia

The Sink Action of Cerebrospinal Fluid in Uremia

The Distributional Nexus of Choroid Plexus to Cerebrospinal Fluid, Ependyma and Brain

Adrenergic-Induced Enhancement of Brain Barrier System Permeability to Small Nonelectrolytes: Choroid Plexus versus Cerebral Capillaries

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Uptake of [14C]urea by the in vivo choroid plexus—cerebrospinal fluid—brain system: identification of sites of molecular sieving

Cited by 40 publications

References 21 publications

The Sink Action of Cerebrospinal Fluid in Uremia

The Sink Action of Cerebrospinal Fluid in Uremia

The Distributional Nexus of Choroid Plexus to Cerebrospinal Fluid, Ependyma and Brain

Adrenergic-Induced Enhancement of Brain Barrier System Permeability to Small Nonelectrolytes: Choroid Plexus versus Cerebral Capillaries

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Uptake of [¹⁴C]urea by the in vivo choroid plexus—cerebrospinal fluid—brain system: identification of sites of molecular sieving