title: [Pathogenesis of sodium and water retention in cirrhosis of the liver].
abstract: Sodium retention is the most common renal abnormality of cirrhosis and eventually leads to the formation of ascites. There is now a strong body of evidence that the arterial vasodilatation, mainly splanchnic, that occurs during liver cirrhosis is a major factor in the pathogenesis of renal sodium and water retention. The arterial vasodilatation and the subsequent hypotension stimulate a baroreceptor-mediated neurohormonal vasoconstrictor and antinatriuretic response in a attempt to compensate the relative underfilling of the circulation. The cause of the arterial vasodilatation is thought to be a circulating factor and several recent studies have implicated an excessive vascular production of nitric oxide (NO). In animal models of cirrhosis administration of NO antagonists corrects the hyperdynamic circulation and improves renal sodium excretion. The treatment of sodium retention is often difficult in liver cirrhosis and it is possible that the identification of a vasodilator substance which can be inhibited could provide a new tool in the therapeutic approach of sodium and water retention in cirrhosis.
authors.affiliation: Department of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA.
authors.forename: P Y
authors.initials: PY
authors.lastname: Martin
mesh_terms: D000818:Animals; D006801:Humans; D006955:Hypernatremia / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology; D008103:Liver Cirrhosis / Q000503:physiopathology*; D009569:Nitric Oxide / Q000502:physiology; D014664:Vasodilation / Q000502:physiology; D014882:Water-Electrolyte Balance / Q000502:physiology*
chemical_list: D009569:Nitric Oxide