Summary
Considerable evidence indicates that regulation of the ionic environment of the brain is coordinated by a central neuroendocrine system capable of affecting the capillary endothelium, the choroid plexus, and the astroglia. All three cell groups are responsible for precise control of brain volume through adjustment of cell water and electrolyte content. With these considerations in mind, we have attempted to elucidate the possible involvement of the central vasopressin (AVP) and atrial natriuretic factor (ANF) systems in the regulation of the water and ion homeostasis of the brain tissue of rats:
Vasopressin-positive vascular connections, investigated by immuno-electronhistochemistry, were found in close or direct contact with brain microvessels. Central administration of AVP (125 ng) or DDAVP (0.5 µg), with or without an accompanying water load, brought about a 1–1.3% water accumulation. Brain oedema caused by experimental subarachnoid haemorrhage had a different course in Wistar and Brattleboro DI rats, the latter being unable to synthetize AVP. These findings suggest that the centrally released AVP leads to brain water accumulation by increasing the water permeability of capillaries, and may facilitate the production of brain oedema in various pathological conditions. On the other hand, central administration of synthetic rat ANF (2 µg) prevented the water accumulation elicited in rat brain by systemic hypoosmolar fluid load, and led to a significant sodium loss from the nervous tissue by altering the capillary sodium permeability. The better understanding of these hormone receptors and their manipulations have exciting clinical implications.
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Dóczi, T., Joó, F., Szerdahelyi, P., Bodosi, M. (1988). Regulation of Brain Water and Electrolyte Contents: the Opposite Actions of Central Vasopressin and Atrial Natriuretic Factor (ANF). In: Isamat, F., Jefferson, A., Loew, F., Symon, L. (eds) Proceedings of the 8th European Congress of Neurosurgery, Barcelona, September 6–11, 1987. Acta Neurochirurgica, vol 43. Springer, Vienna. https://doi.org/10.1007/978-3-7091-8978-8_40
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DOI: https://doi.org/10.1007/978-3-7091-8978-8_40
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