Date of this Version
Published in Taurine 5: Beginning the 21st Century, vol. 526 of the series Advances in Experimental Medicine and Biology, pp. 183–187; doi: 10.1007/978-1-4615-0077-3_23.
The ability to regulate cell volume is an ancient conserved trait present in essentially all species through evolution. The maintenance of a constant cell volume is a homeostatic imperative in animal cells. Changes in cell water content affecting the concentration of intracellular messenger molecules impair the complex signaling network, crucial for cell functioning and intercellular communication. Although the renal homeostatic mechanisms exert a precise control of extracellular fluid osmolarity, this is challenged in a variety of pathological situations. The intracellular volume constancy is continuously compromised by the generation of local and transient osmotic microgradients, associated with nutrients uptake, secretion, cytoskeleton remodeling and transynaptic ionic gradients.1
Cell volume disturbances have particularly dramatic consequences in the brain. The limits to expansion imposed by the rigid skull give narrow margins for the buffering of intracranial volume changes. As expansion occurs, the constraining of small vessels generates episodes of anoxia, ischemia, excitotoxicity, and neuronal death. In extreme conditions, caudal herniation of the brain parenchyma through the foramen magnum affects brain stem nuclei resulting in death by respiratory and cardiac arrest.
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