Controversial role of nitric oxide in hepatic structural and functional injury
2002
S. Sesti | R. Bruno | G. Martino | S. Mazzulla | G. Pitrelli | R. Chimenti
Nitric oxide (NO) may regulate hepatic metabolism directly by causing alterations in hepatocellular (hepatocyte and Kuptfer cell) metabolism and function or indirectly as a result of iU vasodilator properties. NO may be released from the hepatic vascular endothelium, platelets, nerve endings, mast cells, and Kupffer cells as a response to various stimuli such as endotoxemla, ischemia-reperfusion injury, and circulatory shock. It is synthesized by nitric oxide synthase (NOS), which has three distinguishable isofonns: NOS-I (ncNOS), a constitutive isofonn originally isolated from neuronal sources; NOS-2 (iNOS), an inducible isofonn that may generate large quantities of NO and may be Induced In a variety of cell types throughout the body by the action of Inflammatory stimuli; and NOS-3 (ecNOS), a constitutive isofonn originally located in endothelial cells. It is believed that Kupffer cells are the main source of NO during endotoxemic shock and that selective inhibition of this stimulation may have future beneficial therapeutic implications. NO may possess both cytoprotective and cytotoxic properties depending on the amount and the lsofonn of NOS by which It Is produced. The mechanisms by which these properties are regulated are Important In the maintenance of whole body homeostasis and remain to be elucidated.
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