Extracellular volume decreases while cell volume is maintained by ion uptake in rat brain during acute hypernatremia
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1. Regulation of brain extracellular and intracellular water content, regarded as volume, and electrolytes in response to 90 min of hypernatremia has been studied in the cerebral cortex of rats under urethane anaesthetic. 2. Total tissue electrolytes and water were partitioned between extracellular and intracellular compartments based on measurements made in two series of experiments. In one, tissue samples were collected and analysed for total water, Na+, K+ and Cl‐. In the other, tissue extracellular volume fraction, [Na+] and [K+] were measured in situ using ion‐selective microelectrodes. 3. Osmotically induced water loss from cerebral cortex was less than that predicted for ideal osmotic behaviour, revealing a degree of volume regulation, and this regulation was associated with net tissue uptake of Na+, Cl‐ and K+. 4. Total water content was 3.77 g H2O (g dry weight)‐1 in control cortex and this decreased by 7% after 30 min of hypernatremia and then remained relatively stable at this value. Control extracellular water content, based on an extracellular volume fraction of 0.18, was 0.88 g H2O (g dry weight)‐1. Control intracellular water content, estimated as the difference between total and extracellular water contents, was 2.89 g H2O (g dry weight)‐1. After 30 min of hypernatremia, extracellular water content decreased by an average of 27% but intracellular water did not change. This indicates selective regulation of cell volume. By 90 min the extracellular water content had decreased by 47% and the loss in extracellular water content appeared to be accompanied by a roughly equivalent increase in intracellular water content. The intracellular volume increase, however, was not statistically significant. The tortuosity of the extracellular space averaged 1.57 and increased to 1.65 during the hypernatremia. 5. Brain extracellular fluid and plasma [Na+] were roughly equal in control tissue. Both increased by 30 mu equiv (g H2O)‐1 as a result of the hypernatremia, although extracellular [Na+] lagged behind the plasma value during much of the first 60 min of hypernatremia. Extracellular [K+] was homeostatically regulated at 3 mu equiv (g H2O)‐1 independent of changes in plasma electrolytes. 6. Estimates of extracellular and intracellular ion content (mu equiv (g dry weight)‐1) indicate that extracellular Na+, Cl‐ and K+ content decreased during hypernatremia, by 32, 21 and 42% respectively, whereas intracellular ion content increased by 100, 169 and 5% respectively. 7. It is concluded that during acute hypernatremia the extracellular space decreases in volume through the loss of water and electrolytes while the intracellular compartment maintains its water content and gains electrolytes.(ABSTRACT TRUNCATED AT 400 WORDS)
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The effects of osmotic states on seizure susceptibility are in part due to an osmotic gradient across the blood-brain barrier, leading to water movement and changes in extracellular space.
“effects in part due to an osmotic gradient across the blood-brain barrier, leading to respective movements of water and changes of extracellular space (Cserr et al. 1991;Silver et al. 1996;Verkman, 2005).”
From Significance of SGK1 in the regulation of neuronal function (2010) · cites this paper as Cserr et al. 1991
The paper’s abstract (pp. 277–295; passage 3) reports osmotically induced water loss from rat cerebral cortex during acute hypernatremia. It concludes that extracellular space decreases as water and electrolytes are lost (passage 4). The available text does not establish an osmotic gradient specifically across the blood–brain barrier or link these changes to seizure susceptibility. (LLM, conf=0.84)
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Significance of SGK1 in the regulation of neuronal function
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- Authors
- Cserr, H. F., DePasquale, M., Nicholson, C., Patlak, C. S., Pettigrew, K. D., & Rice, M. E.
- Affiliations
- Brown University (US)
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 1991-10
- Volume
- 442
- Issue
- 1
- Pages
- 277-295
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC1179889
- OpenAlex
- W2005896706
- Cited by
- 141
- References
- 0
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 1 · 2019: 4 · 2018: 3 · 2016: 4 · 2014: 2 · 2013: 2 · 2012: 4
- FWCI
- 13.35
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ns011050-17, 1f32ns007745-01)
- National Institute of Neurological Disorders and Stroke (NS 11050, NS 13742, P01NS013742, NS-07745)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Electrolyte and hormonal disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Cerebrospinal fluid and hydrocephalus
- Keywords
- hypernatremia, extracellular volume, intracellular fluid volume, cerebral cortex, sodium uptake, potassium homeostasis, chloride, ion-selective microelectrodes, brain electrolytes, volume regulation, rat brain, urethane anesthesia, plasma sodium, plasma potassium, plasma chloride
- MeSH terms
- Animals, Brain, Brain Chemistry, Extracellular Space, Hypernatremia, Intracellular Fluid, Osmolar Concentration, Potassium, Sodium, Water-Electrolyte Balance, Rats
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