Urotensin II: a novel vasoactive mediator linked to chronic liver disease and portal hypertension

Kemp, William; Krum, Henry; Colman, John; Bailey, Michael; Yandle, Tim G.; Richards, Mark; Roberts, Stuart K.

doi:10.1111/j.1478-3231.2007.01539.x

Cited by 30 publications

(42 citation statements)

References 42 publications

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“…The observation that basal hemodynamics and general vasopressor responsiveness are unaltered in UT knockout mice supports the suggestion that the receptor is functionally silent under basal conditions, but this may change in cardiovascular diseases (13). In addition to elevated levels in patients with heart failure, systemic hypertension, diabetes mellitus, and renal failure (14,15), increased plasma UII levels have been reported in patients with cirrhosis (16,17).…”

Section: Introductionsupporting

confidence: 55%

“…Recently, several studies have shown that UII plasma levels are increased in patients with liver cirrhosis and portal hypertension (16,17). The UII plasma levels are correlated negatively with mean arterial pressure and positively with portal pressure and severity of liver disease, as assessed using the Child-Pugh score (16,17).…”

Section: Discussionmentioning

confidence: 99%

“…The UII plasma levels are correlated negatively with mean arterial pressure and positively with portal pressure and severity of liver disease, as assessed using the Child-Pugh score (16,17). However, the site of increased production of UII in patients with chronic liver disease remains unclear (9).…”

Section: Discussionmentioning

confidence: 99%

“…In apparent variance with our data, Leifeld et al have shown by immunohistochemistry that there was no significant difference in UII/UT between cirrhotic and control liver. There are likely to be many reasons for this disparity, including the diverse population group, rapid degradation of UII after its secretion, and marked differences in sensitivity and possibly specificity, between the UT assays (16,17,22), and its probable autocrine/ paracrine mechanism of action (23,24). Other differences, besides etiology, are the absence of portal hypertension and plasma UII measurements in the study of Leifeld et al Patients with cirrhosis and ascites (as confirmation of portal hypertension) have higher UII levels than those without ascites (17).…”

Section: Discussionmentioning

confidence: 99%

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Increased expression of urotensin II and GPR14 in patients with cirrhosis and portal hypertension

Liu

Chen²,

Wang³

et al. 2010

Int J Mol Med

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Abstract. Urotensin II (UII) and its receptor (UT or GPR14) are involved in liver fibrosis and portal hypertension. Nevertheless, expression of the UII/UT system in the liver of patients with portal hypertension has not been elucidated. UII and UT gene expression were quantified in liver biopsy samples from patients with hepatitis-B-virus-associated cirrhosis and portal hypertension, and from normal controls by using quantitative real-time PCR. The liver distribution of UT was determined by means of immunohistochemistry and immunofluorescence. Western blot analysis was used to assess liver levels of UT. Simultaneously, we measured intraoperative free portal venous pressure (FPVP) and collected plasma for UII measurement by ELISA. UT expression at the mRNA and protein level was enhanced significantly in the liver of patients with cirrhosis and portal hypertension, compared with that in healthy controls. UT protein expression was concentrated mainly in the Kupffer cells and sinusoidal endothelial cells. In cirrhotic tissue, UII gene expression was increased 5-fold in comparison to that in normal liver tissue. Plasma UII level was higher in cirrhotic patients compared with controls and was correlated with FPVP (r=0.807; P<0.001) and UII mRNA in the liver (r=0.802; P<0.001). These findings suggest that the intrahepatic UII/UT system has an important pathophysiological role in cirrhosis and portal hypertension.

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Section: Introductionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Increased expression of urotensin II and GPR14 in patients with cirrhosis and portal hypertension

Liu

Chen²,

Wang³

et al. 2010

Int J Mol Med

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“…Furthermore, UII has an inotropic effect in humans and rats [8]. Increased plasma UII concentration was observed in patients with diabetes mellitus and end-stage kidney disease [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Is plasma urotensin II concentration an indicator of myocardial damage in patients with acute coronary syndrome?

Babińska¹,

Holecki²,

Prochaczek³

et al. 2012

aoms

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A b s t r a c tIntroduction: Urotensin II (UII) is a vasoactive peptide secreted by endothelial cells. Increased plasma UII concentration was observed in patients with heart failure, liver cirrhosis, diabetic nephropathy and renal insufficiency. In patients with myocardial infarction both increased and decreased plasma UII concentrations were demonstrated. The aim of this study was to analyze whether plasma UII concentration reflects the severity of acute coronary syndrome (ACS). Material and methods: One hundred and forty-nine consecutive patients with ACS, without age limit, were enrolled in the study. In all patients plasma concentration of creatinine, creatine kinase isoenzyme MB (CK-MB), troponin C, N-terminal prohormone of brain natriuretic peptide (NT-pro BNP), and UII were assessed, and echocardiography was performed in order to assess the degree of left ventricular hypertrophy, ejection fraction (EF) and mass (LVM). Results: In patients with the highest risk (TIMI 5-7) plasma UII concentration was significantly lower than in those with low risk (TIMI 1-2): 2.61 ±1.47 ng/ml vs. 3.60 ±2.20 ng/ml. Significantly lower plasma UII concentration was found in patients with increased concentration of troponin C (2.60 ±1.52 ng/ml vs. 3.41 ±2.09 ng/ml). There was a significant negative correlation between plasma UII concentration and TIMI score or concentration of troponin C, but not CK-MB. Borderline correlation between plasma UII and ejection fraction (R = 0.157; p = 0.063) or NT-proBNP (R = -0.156; p = 0.058) was found. Conclusions: Decreased plasma urotensin II concentration in patients with ACS could be associated with more severe injury of myocardium.

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Pathophysiology of Portal Hypertension

Iwakiri

Groszmann

2020

The Liver

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Portal hypertension is a major complication of liver disease, which results from a variety of pathological conditions that increase the resistance to the portal blood flow into the liver. The primary cause of portal hypertension in cirrhosis is an increase in intrahepatic vascular resistance due to massive structural changes associated with fibrosis and increased vascular tone in the hepatic microcirculation. As portal hypertension develops, the formation of collateral vessels and arterial vasodilation progress, which results in increased blood flow to the portal circulation. Eventually the hyperdynamic circulatory syndrome develops, leading to esophageal varices or ascites. This review article will summarize the factors that increase 1) intrahepatic vascular resistance and 2) the blood flow in the splanchnic and systemic circulations in liver cirrhosis. Finally, the future directions of basic/clinical research in portal hypertension will be discussed.

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Urotensin II: a novel vasoactive mediator linked to chronic liver disease and portal hypertension

Abstract: Serum UII is elevated in patients with CLD, and is associated with the severity of the underlying liver disease and the degree of portal hypertension. Baseline levels can predict future complications such as refractory ascites and patient survival.

Cited by 30 publications

References 42 publications

Increased expression of urotensin II and GPR14 in patients with cirrhosis and portal hypertension

Increased expression of urotensin II and GPR14 in patients with cirrhosis and portal hypertension

Is plasma urotensin II concentration an indicator of myocardial damage in patients with acute coronary syndrome?

Pathophysiology of Portal Hypertension

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