TY - JOUR
T1 - Mechanisms counteracting swelling in brain cells during hyponatremia
AU - Pasantes-Morales, Herminia
AU - Franco, Rodrigo
AU - Ordaz, Benito
AU - Ochoa, Lenin D.
N1 - Funding Information:
Research in our laboratory was supported by grants IN204900 from DGAPA-UNAM and 34886-M from CONACYT, México.
PY - 2002
Y1 - 2002
N2 - Water gain in the brain consequent to hyponatremia is counteracted by mechanisms that initially include a compensatory displacement of liquid from the interstitial space to cerebrospinal fluid and systemic circulation and subsequently an active reduction in cell water accomplished by extrusion of intracellular osmolytes to reach osmotic equilibrium. Potassium (K+), chloride (Cl-), amino acids, polyalcohols, and methylamines all contribute to volume regulation, with a major contribution of ions at the early phase and of organic osmolytes at the late phase of the regulatory process. Experimental models in vitro show that osmolyte fluxes occur via leak pathways for organic osmolytes and separate channels for Cl- and K+. Osmotransduction signaling cascades for Cl- and taurine efflux pathways involve tyrosine kinases and phosphoinositide kinases, while Ca2+ and serine-threonine kinases modulate K+ pathways. In-depth knowledge of the cellular and molecular adaptive mechanisms of brain cells during hyponatremia contributes to a better understanding of the associated complications, including the risks of inappropriate correction of the hyponatremic condition.
AB - Water gain in the brain consequent to hyponatremia is counteracted by mechanisms that initially include a compensatory displacement of liquid from the interstitial space to cerebrospinal fluid and systemic circulation and subsequently an active reduction in cell water accomplished by extrusion of intracellular osmolytes to reach osmotic equilibrium. Potassium (K+), chloride (Cl-), amino acids, polyalcohols, and methylamines all contribute to volume regulation, with a major contribution of ions at the early phase and of organic osmolytes at the late phase of the regulatory process. Experimental models in vitro show that osmolyte fluxes occur via leak pathways for organic osmolytes and separate channels for Cl- and K+. Osmotransduction signaling cascades for Cl- and taurine efflux pathways involve tyrosine kinases and phosphoinositide kinases, while Ca2+ and serine-threonine kinases modulate K+ pathways. In-depth knowledge of the cellular and molecular adaptive mechanisms of brain cells during hyponatremia contributes to a better understanding of the associated complications, including the risks of inappropriate correction of the hyponatremic condition.
KW - Hyposmolarity
KW - Regulatory volume decrease
KW - Taurine
KW - Volume regulation
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U2 - 10.1016/S0188-4409(02)00353-3
DO - 10.1016/S0188-4409(02)00353-3
M3 - Review article
C2 - 12031627
AN - SCOPUS:0036113181
VL - 33
SP - 237
EP - 244
JO - Archives of Medical Research
JF - Archives of Medical Research
SN - 0188-4409
IS - 3
ER -