Increased plasma levels of neuropeptide Y in hepatorenal syndrome

Úriz, J.; Ginès, Pere; Ortega, Rolando; Jiménez, Wladimiro; Cárdenas, Andrés; Calahorra, B.; Sort, Pau; Fernández, Javier; Bataller, Ramón; Arroyo, Vicente; Rivera, Francisca; Rodés, Juan

doi:10.1016/s0168-8278(01)00286-0

Cited by 22 publications

(12 citation statements)

References 40 publications

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“…The NPY serum levels observed in our normal rats are similar to those found in other studies in rats (32) and slightly higher than those observed in humans (35,36). We propose that the decrease in serum NPY levels observed in BDL rats may be due to reduced secretion of NPY by the neural tissue of the central and peripheral nervous system (38).…”

Section: Discussionsupporting

confidence: 89%

“…In support of our findings, a study has demonstrated that decreased plasma NPY levels are correlated with the severity of liver damage (similar to BDL) (2), which may be the reason for hemodynamic and ascitic formation changes in liver cirrhosis patients (19). On the other hand, increased plasma levels of NPY were detected in patients with hepatorenal syndrome (36). No difference in circulating NPY levels was observed between normal patients and patients with fulminant hepatic failure (34).…”

Section: Discussionmentioning

confidence: 90%

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Neuropeptide Y inhibits biliary hyperplasia of cholestatic rats by paracrine and autocrine mechanisms

DeMorrow

Meng

Venter

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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Biliary homeostasis is regulated by several factors through autocrine/paracrine signaling. NPY inhibits cholangiocarcinoma growth; however, no information exists regarding the autocrine/paracrine role of NPY on biliary hyperplasia during cholestasis. The aims of this study were to determine: 1) the expression of NPY and Y 1-Y5 in cholangiocytes and 2) the paracrine/autocrine effects of NPY on cholangiocyte proliferation. Normal or bile duct ligation (BDL) rats were treated with NPY, neutralizing anti-NPY antibody, or vehicle for 7 days. NPY and NPY receptor (NPYR) expression was assessed in liver sections and isolated cholangiocytes. NPY secretion was assessed in serum and bile from normal and BDL rats, as well as supernatants from normal and BDL cholangiocytes and normal rat cholangiocyte cell line [intrahepatic normal cholangiocyte culture (NRICC)]. We evaluated intrahepatic bile ductal mass (IBDM) in liver sections and proliferation in cholangiocytes. With the use of NRICC, the effects of NPY or anti-NPY antibody on cholangiocyte proliferation were determined. The expression of NPY and all NPYR were increased after BDL. NPY levels were lower in serum and cholangiocyte supernatant from BDL compared with normal rats. NPY secretion from NRICC was detected at both the basolateral and apical domains. Chronic NPY treatment decreased proliferating cellular nuclear antigen (PCNA) expression and IBDM in BDL rats. Administration of anti-NPY antibody to BDL rats increased cholangiocyte proliferation and IBDM. NPY treatment of NRICC decreased PCNA expression and increased the cell cycle arrest, whereas treatment with anti-NPY antibody increased proliferation. Therapies targeting NPY-mediated signaling may prove beneficial for the treatment of cholangiopathies. biliary epithelium; neurotransmitters; proliferation; cell cycle CHOLANGIOCYTES ARE THE TARGET cells in cholangiopathies such as primary biliary cirrhosis and primary sclerosing cholangitis (4).During the course of these diseases and in many other forms of liver injury, a balance between cholangiocyte proliferation and loss is critical for the maintenance of the homeostasis of biliary mass (4). Effort has gone into identifying the factors regulating biliary loss/proliferation to identify potential therapeutic targets for the maintenance of biliary mass during liver diseases.Biliary mass is coordinately regulated by a number of growth factors and hormones during normal and cholestatic states by both autocrine and paracrine signaling (5, 12, 13, 23, 28). After bile duct ligation (BDL), cholangiocytes secrete increased amounts of growth factors such as vascular endothelial growth factor (VEGF) and nerve growth factor (NGF) stimulating biliary proliferation (12, 13). Conversely, proliferating cholangiocytes secrete increased amounts of serotonin (23) and melatonin (28) that inhibit cholangiocyte proliferation. Serotonin and melatonin may be secreted by cholangiocytes to prevent overt biliary proliferation in response to cholestasis.Neuropeptide Y (NPY) is a neurotransm...

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 90%

Neuropeptide Y inhibits biliary hyperplasia of cholestatic rats by paracrine and autocrine mechanisms

DeMorrow

Meng

Venter

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Plasma renin activity, aldosterone, and norepinephrine were determined using previously described methods. 15 Statistical Analysis. Comparisons of the variables in the same group were performed using the paired Student's t test and Wilcoxon test for continuous data and the chi-square test and Fisher test for categorical data.…”

Section: Methodsmentioning

confidence: 99%

Effects of contrast media on renal function in patients with cirrhosis: A prospective study

et al. 2004

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Patients with cirrhosis are frequently submitted to radiological procedures that require the administration of contrast media. Contrast media is a well-known cause of renal failure, particularly in the presence of some predisposing conditions. However, it is not known whether cirrhosis constitutes a risk factor for contrast media-induced renal failure. The aim of this study was to assess the possible nephrotoxicity of contrast media in patients with cirrhosis. In a first protocol, renal function was evaluated with sensitive methods (glomerular filtration rate using iothalamate I 125 clearance and renal plasma flow using iodohippurate I 131 clearance) before and 48 hours after the administration of contrast media in 31 patients with cirrhosis (20 with ascites, 5 with renal failure). Solute-free water clearance, urine sodium, prostaglandins, and markers of tubular damage were also measured. The administration of contrast media was not associated with significant changes in renal function tests, neither in the whole group of patients nor in patients with ascites or renal failure. Urinary prostaglandin E2 and N-acetyl-␤-D-glucosaminidase increased significantly, but sodium and solute-free water excretion remained unchanged. In a second protocol, a different series of 60 patients with cirrhosis and renal failure were examined prospectively. No patient had renal failure due to contrast media. Only in 1 patient with septic shock was contrast media a possible contributing factor. In conclusion, the administration of contrast media is not associated with adverse effects on renal function in patients with cirrhosis. Cirrhosis does not appear to be a risk factor for the development of contrast media-induced nephrotoxicity.

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“…The pronounced effect of exogenous NPY on α 1 -adrenergic mesenteric contraction in PVL rats suggested in vivo a lack of amplification of contractile signalling by the absence of NPY in these vessels 157. Yet, the relevance of elevated NPY levels at least in advanced human cirrhosis remains to be clarified in this context 158. Nevertheless, these studies underline the importance of contractile signalling in VSM cells, which may be endothelium-independently dysregulated at different levels in portal hypertension.…”

Section: Mechanisms Of Vascular Hypocontractility and Vasodilation Inmentioning

confidence: 97%

Mechanisms of extrahepatic vasodilation in portal hypertension

Hennenberg

Trebicka

Sauerbruch

et al. 2008

Gut

148

161

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In liver cirrhosis, abnormal persistent extrahepatic vasodilation leads to hyperdynamic circulatory dysfunction which essentially contributes to portal hypertension. Since portal hypertension is a major factor in the development of complications in cirrhosis, the mechanisms underlying this vasodilation are of paramount interest. Extensive studies performed in cirrhotic patients and animals revealed that this vasodilation is associated on the one hand with enhanced formation of vasodilators, and on the other hand with vascular hyporesponsiveness to vasoconstrictors. The latter phenomenon has been termed "vascular hypocontractility". It is caused by a combination of different mechanisms and factors described in this review.

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Increased plasma levels of neuropeptide Y in hepatorenal syndrome

Cited by 22 publications

References 40 publications

Neuropeptide Y inhibits biliary hyperplasia of cholestatic rats by paracrine and autocrine mechanisms

Neuropeptide Y inhibits biliary hyperplasia of cholestatic rats by paracrine and autocrine mechanisms

Effects of contrast media on renal function in patients with cirrhosis: A prospective study

Mechanisms of extrahepatic vasodilation in portal hypertension

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