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NCX-1000: a liver-specific NO donor

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Abstract

Recent advances in the knowledge of the pathophysiology of portal hypertension show that cirrhotic liver exhibits endothelial dysfunction of sinusoidal endothelial cells. This alteration results in a defective or absent vasodilatory response to acetylcholine and in insufficient nitric oxide (NO) production by endothelial NO synthase in the intrahepatic vascular bed. Such deficient NO production increases hepatic vascular tone, and may decrease the intrahepatic vasodilatory adaptive response to sudden increases in blood flow13. Therefore, drugs that deliver NO to the intrahepatic circulation, such as nitrates, should be able to compensate for reduced NO generation and reduce portal pressure gradient. For this reason vasodilators have been studied in recent years as a possible alternative to β-blockers in the pharmacologic treatment of portal hypertension.

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© 2004 Springer Science+Business Media Dordrecht

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Fiorucci, S., Antonelli, E., Morelli, A. (2004). NCX-1000: a liver-specific NO donor. In: Groszmann, R.J., Bosch, J. (eds) Portal Hypertension in the 21st Century. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-1042-9_12

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  • DOI: https://doi.org/10.1007/978-94-007-1042-9_12

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-3774-7

  • Online ISBN: 978-94-007-1042-9

  • eBook Packages: Springer Book Archive

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