Circulating adrenomedullin in cirrhosis

Endothelial nitric oxide synthase is not essential for the development of fibrosis and portal hypertension in bile duct ligated mice

“…However, consistent with our portal pressure findings, we found no significant differences after BDL in HO1 or HO2 protein or endothelin receptor binding between WT and eNOS KO mice. We have no indication as to which if any of other known vasoactive agents (38–46) could be compensating for the lack of eNOS in these KO mice, although there is some evidence that nNOS may be partly compensating (47).…”

Nitric oxide synthase 1 is partly compensating for nitric oxide synthase 3 deficiency in nitric oxide synthase 3 knock‐out mice and is elevated in murine and human cirrhosis

“…Peripheral vasodilation and dilation of the mesenteric vascular bed are involved in the pathogenesis of the hyperdynamic circulation syndrome that parallels portal hypertension (1). The basic principles of the pathophysiology of portal hypertension are not completely understood but an imbalance between vasoconstrictors and vasodilators has been shown in numerous studies (2, 6, 35, 36). NO seems to play a central role as a vasodilator in portal hypertension with or without cirrhosis (10, 37–39).…”

“…Cirrhosis of the liver and associated portal hypertension are characterized by low systemic vascular resistance, low blood pressure and increased cardiac output (1). Almost all vasoactive systems are activated or increased in this state of hyperdynamic circulation and many studies have stressed the importance of endothelial factors, such as endothelins, prostaglandins, endogenous cannabinoids, adrenomedullin and nitric oxide (NO) (2–10). The role of NO in arterial vasodilation has been shown in various animal studies.…”