The brain in hyponatremia: both culprit and victim

Semin Nephrol. 2009 May;29(3):196-215. doi: 10.1016/j.semnephrol.2009.03.021.

Abstract

Abnormalities in thirst and vasopressin (AVP) release play key roles in the genesis of hyponatremia; both processes are under the control of osmoreceptive neurons in the central nervous system (CNS). The acute development of hyponatremia in turn leads to profound cerebral edema, whereas treatment of chronic hyponatremia can be associated with osmotic demyelination syndrome (ODS). The brain is thus both "culprit" and "victim" in hyponatremia. This review summarizes recent advances in the understanding of osmoreception in the brain, the CNS response to acute and chronic hyponatremia, and the pathophysiology of ODS.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Brain / physiopathology*
  • Demyelinating Diseases / physiopathology
  • Humans
  • Hyponatremia / physiopathology*
  • Hyponatremia / therapy*
  • Models, Biological
  • Osmosis
  • Thirst
  • Vasopressins / physiology

Substances

  • Vasopressins