Elsevier

Journal of Hepatology

Volume 34, Issue 6, June 2001, Pages 936-939
Journal of Hepatology

Editorial
Heme oxygenase: protective enzyme or portal hypertensive molecule?

https://doi.org/10.1016/S0168-8278(01)00090-3Get rights and content

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      Portal hypertension–associated hyporeactivity to vasoconstrictors is caused mainly by NO (reviewed in [9–11]). The molecular mechanisms of NO-induced portal hypertensive SMC hyporesponsiveness are not well understood [10,20]. In normal SMC, NO stimulates soluble guanylyl cyclase to produce the second messenger, cyclic 3′,5′-guanosine monophosphate (cGMP) [22].

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      However, this would be detrimental because increased production of CO in splanchnic organs may contribute to the development and maintenance of an increased splanchnic blood flow and hyperdynamic circulation associated with PHT [66]. Therefore, in PHT, HO might be both a protective enzyme and a portal hypertensive molecule [67]. In relation to HO-2, the constitutive isoform of HO, the only chemical inducers identified are adrenal glucocorticoids [68].

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