Organic osmolytes in hyponatremia and ammonia toxicity
- PMID: 20195726
- DOI: 10.1007/s11011-010-9170-5
Organic osmolytes in hyponatremia and ammonia toxicity
Abstract
Hyperammonemia (HA) is a major and commonly observed feature of hepatic encephalopathy. Furthermore, hyponatremia is an important pathogenetic factor in patients with hepatic encephalopathy. Both conditions have some features in common, such as the release of organic osmolytes, which might be an adaptive mechanism against cell swelling. However, the consequence of a possible relationship between osmoregulatory response in hyperammonemia and hyponatremia is not completely understood. This review gives a short introduction into the pathogenesis of hepatic encephalopathy and hyponatremia. For a comparison of both pathological events, some basics on cellular osmo- and volume regulation are explained, in particular as the mechanisms involved in the adaption of the cell to volume changes can be different under both pathological conditions. The role of brain glutamine and organic osmolytes in hyponatremia and hyperammonemia and their combination are discussed based on findings in experimental animal models, and finally on data obtained from primary astrocytes in culture. The observations that the decrease of brain organic osmolytes in astrocytes not adequately compensate for an increased intracellular osmolarity caused by glutamine are consistent with results obtained after chronic hyponatremia in rats, in which the release of osmolytes does not protect from ammonia-induced brain edema. Furthermore, a decrease in intracellular osmolarity is attributed both to the release and a reduced de novo synthesis of amino acids.
Similar articles
-
Ammonia toxicity under hyponatremic conditions in astrocytes: de novo synthesis of amino acids for the osmoregulatory response.Neurochem Int. 2005 Jul;47(1-2):39-50. doi: 10.1016/j.neuint.2005.04.005. Neurochem Int. 2005. PMID: 15908044
-
Chronic hyponatremia exacerbates ammonia-induced brain edema in rats after portacaval anastomosis.J Hepatol. 1998 Oct;29(4):589-94. doi: 10.1016/s0168-8278(98)80154-2. J Hepatol. 1998. PMID: 9824268
-
RNA oxidation and zinc in hepatic encephalopathy and hyperammonemia.Metab Brain Dis. 2009 Mar;24(1):119-34. doi: 10.1007/s11011-008-9125-2. Epub 2009 Jan 16. Metab Brain Dis. 2009. PMID: 19148713 Review.
-
Inhibitors of the mitochondrial permeability transition reduce ammonia-induced cell swelling in cultured astrocytes.J Neurosci Res. 2009 Sep;87(12):2677-85. doi: 10.1002/jnr.22097. J Neurosci Res. 2009. PMID: 19382208
-
An update on the role of brain glutamine synthesis and its relation to cell-specific energy metabolism in the hyperammonemic brain: further studies using NMR spectroscopy.Neurochem Int. 2005 Jul;47(1-2):19-30. doi: 10.1016/j.neuint.2005.04.003. Neurochem Int. 2005. PMID: 15916833 Review.
Cited by
-
Differential impact of hyponatremia and hepatic encephalopathy on health-related quality of life and brain metabolite abnormalities in cirrhosis.J Hepatol. 2013 Sep;59(3):467-73. doi: 10.1016/j.jhep.2013.04.023. Epub 2013 May 7. J Hepatol. 2013. PMID: 23665182 Free PMC article.
-
MicroRNA-Mediated Metabolic Reprograming in Renal Cancer.Cancers (Basel). 2019 Nov 20;11(12):1825. doi: 10.3390/cancers11121825. Cancers (Basel). 2019. PMID: 31756931 Free PMC article.
-
Enzymatic analysis of α-ketoglutaramate--a biomarker for hyperammonemia.Talanta. 2012 Oct 15;100:7-11. doi: 10.1016/j.talanta.2012.08.022. Epub 2012 Aug 24. Talanta. 2012. PMID: 23141304 Free PMC article.
-
Primary carnitine deficiency and pivalic acid exposure causing encephalopathy and fatal cardiac events.J Inherit Metab Dis. 2013 Jan;36(1):35-41. doi: 10.1007/s10545-012-9488-8. Epub 2012 May 8. J Inherit Metab Dis. 2013. PMID: 22566287
-
Hyponatremia in Patients with Cirrhosis of the Liver.J Clin Med. 2014 Dec 31;4(1):85-101. doi: 10.3390/jcm4010085. J Clin Med. 2014. PMID: 26237020 Free PMC article. Review.
References
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical