The Roles of Angiotensin II Receptors in the Portosystemic Collaterals of Portal Hypertensive and Cirrhotic Rats

Chang, Ching Chih; Wang, Sun Sang; Lee, Fa Yauh; Teng, Tzu Hua; Lee, Jing Yi; Lin, Han Chieh; Chuang, Chiao Lin; Lee, Shou Dong

doi:10.1159/000332347

Cited by 5 publications

(4 citation statements)

References 73 publications

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“…BDL is a well-established technique to induce secondary biliary cirrhosis with NO over-expression and hepatopulmonary syndrome [36]. It has been applied in our previous studies addressing the vasoresponsiveness in cirrhosis [37], [38]. Hepatotoxins, such as carbon tetrachloride (CCl 4 ), have also been used to elicit cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Diabetes Diminishes the Portal-Systemic Collateral Vascular Response to Vasopressin via Vasopressin Receptor and Gα Proteins Regulations in Cirrhotic Rats

Lee¹,

Huo

Wang

et al. 2013

PLoS ONE

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Liver cirrhosis may lead to portal-systemic collateral formation and bleeding. The hemostatic effect is influenced by the response of collateral vessels to vasoconstrictors. Diabetes and glucose also influence vasoresponsiveness, but their net effect on collaterals remains unexplored. This study investigated the impact of diabetes or glucose application on portal-systemic collateral vasoresponsiveness to arginine vasopressin (AVP) in cirrhosis. Spraque-Dawley rats with bile duct ligation (BDL)-induced cirrhosis received vehicle (citrate buffer) or streptozotocin (diabetic, BDL/STZ). The in situ collateral perfusion was done after hemodynamic measurements: Both were perfused with Krebs solution, D-glucose, or D-glucose and NaF, with additional OPC-31260 for the BDL/STZ group. Splenorenal shunt vasopressin receptors and Gα proteins mRNA expressions were evaluated. The survival rate of cirrhotic rats was decreased by STZ injection. The collateral perfusion pressure changes to AVP were lower in STZ-injected groups, which were reversed by OPC-31260 (a V2R antagonist) and overcome by NaF (a G protein activator). The splenorenal shunt V2R mRNA expression was increased while Gα proteins mRNA expressions were decreased in BDL/STZ rats compared to BDL rats. The Gαq and Gα11 mRNA expressions also correlated with the maximal perfusion pressure changes to AVP. Diabetes diminished the portal-systemic collateral vascular response to AVP in rats with BDL-induced cirrhosis, probably via V2 receptor up-regulation and Gα proteins down-regulation.

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Section: Discussionmentioning

confidence: 99%

Diabetes Diminishes the Portal-Systemic Collateral Vascular Response to Vasopressin via Vasopressin Receptor and Gα Proteins Regulations in Cirrhotic Rats

Lee¹,

Huo

Wang

et al. 2013

PLoS ONE

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“…The main reason could be that some spontaneous shunts were retained intra-operatively, thus further reducing the portal blood flow and hepatic sinusoidal pressure and increasing the hepatic artery flow velocity [23,24]. Moreover, the vasodilator mediators, including nitric oxide, were inactivated in liver due to shunts [25,26]. In our study, HAF and SMVF increased significantly after SD-PDPV procedure, due to the decreasing of PVF to liver.…”

Section: Uni-and Multivariate Analysis Of Predictors For Postoperativmentioning

confidence: 50%

Effects of selective double portazygous disconnection and devascularization on hemodynamics of the portal venous system

et al. 2014

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Aim: Selective double portazygous disconnection with preserving vagus (SDPDPV) is currently used for the therapy of portal hypertension. Doppler ultrasonography (DU) has been proposed for non-invasive evaluation of splanchnic hemodynamics, but the effect of SDPDPV on portal vein (PV) hemodynamics has not been analyzed with DU. This was the aim of the study. Material and methods: Two hundred and thirty six patients with cirrhotic portal hypertension who underwent either SDPDPV or pericardial devascularization with splenectomy (PDS) for variceal bleeding were enrolled. The hemodynamics parameter, operation-relevant information, change of lavatory examination data, postoperative complications, and clinical outcomes were analyzed. Results: The free portal pressure (FPP) in the SDPDPV group was significantly lower than the PDS group after operation (p<0.05). Velocities and blood flow of PV after SDPDPV decreased; however, when the hepatic artery (HA) and superior mesenteric vein (SMV) increased, the differences were significant (p<0.05). The correlation between the decreased FPP and changed blood flow of portal vein(PVF), hepatic artery (HAF) or superior mesenteric vein (SMVF) was significant (p<0.05) after SDPDPV. The difference between pre and postoperative values of portal congestion index (CI) in SDPDPV was significant (p<0.05). Occurrences or development of postoperative rebleeding showed a great difference between the two groups (p< 0.05). PVF and SMVF were significant independent indicators of postoperative rebleeding (p< 0.05). Conclusions: Compared with the PDS, the SDPDPV apparently decreased the blood velocity and blood flow of PV, and increased that of HA and SMV which has a beneficial effect on hepatic function and encourages the controlof the recurrent bleeding from varices. PVF and SMVF may be value indicators in predicting postoperative rebleeding.

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“…Role of RAAS on portal pressure provides a new therapeutic alternative [35]. Animal model studies and clinical trials have shown that blockade of Ang II type 1 receptor (AT1R) significantly reduced portal perfusion pressure and HVPG [36][37][38][39]. ACE inhibitor also effects to reduce portal pressure in cirrhotic patients [40].…”

Section: Raasmentioning

confidence: 99%

Vasoactive Substances and Inflammatory Factors in Progression of Liver Cirrhosis with Portal Hypertension

Lu¹,

Li²,

Lü³

et al. 2013

Hepatic Surgery

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Portal hypertension PH , a detrimental complication of many diseases, is abnormalities in pre-, intra-or post-hepatic portal venous system. Intrahepatic PH is the most common type, which is mainly cause by liver cirrhosis [ ], liver cancer, and sometimes intrahepatic vascular abnormalities [ ].Hepatic venous pressure gradient HVPG is the difference between wedged hepatic venous pressure and infra vena cava pressure. PH is defined as an HVPG higher than mmHg [ ]. According to absence or presence of complications splenomegaly and hypersplenism, esophageal varices and ascites , PH can be classified into compensated or decompensated phase. Meanwhile, an HVPG higher than mmHg has been considered as a direct predictor of decompensation and a -year-follow-up study showed the significant worse longterm survival when HVPG ＞ mmHg [ -].In cirrhotic PH, increased intrahepatic vascular resistance IHVR is the primary factor [ , ] and subsequently increased portal vein inflow PVI worsens the situation of PH patients. This review will focus on the physiopathological changes happened in PH.. Contrastingly, extrahepatic NO is increased in PH patients. A clinical trial has shown that serum nitrate level was positively correlated with clinical presentation, e.g. pulse rate, jaundice, hepatic encephalopathy, lower limb edema and esophageal varices [ ]. It is well established that NO results in dilation of splanchnic and systemic circulation as a powerful vasodilator and blood level of NO is increased as PH progresses [ -]. Administration of CCl to eNOS -/-mice also led to an elevated NO production, which is eNOS independent [ ]. Another study suggested that iNOS might be involved [ ]. . . Carbon monoxideCarbon monoxide CO , a vasodilator producing by heme oxygenases HOs from heme [ ], changes as HO-expression altered in PH patients [ , ], which shares the same characters with NO [ ]. Expression of intrahepatic HO-and -decreased in cirrhotic rats than that in normal ones. In situ perfusion with CO-releasing molecule-, which leads to relaxation of hepatic stellate cells, and HO-inducer hemin could attenuated increased IHVR. ZnPP caused a higher IHVR attributing to inhibition of intrahepatic HOin cirrhotic liver[ ].But things are different in splanchnic and systemic circulation. Reportedly, portal vein pressure PVP was significantly higher in bile-duct-ligated rats than that in sham group. Meanwhile, mRNA and protein level of HO-was also elevated significantly in lung [ ].A clinical study has shown an activated HO/CO system in cirrhotic patients while the HOactivity and plasma level of CO were related with the severity of PH [ ]. Arterial blood gas analysis showed an increase of COHb in bile-duct-ligated rats which could be reversed by ZnPP [ ]. HO-could promote expression of VEGF and thereafter lead to formation of collateral vessels and higher splanchnic circulation [ ]. . . EndothelinEndothelin-ET-is the most powerful vasoconstrictor in ETs family [ ], which is primarily synthesized and acts in liver mainly in a paracrine fashion ...

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The Roles of Angiotensin II Receptors in the Portosystemic Collaterals of Portal Hypertensive and Cirrhotic Rats

Cited by 5 publications

References 73 publications

Diabetes Diminishes the Portal-Systemic Collateral Vascular Response to Vasopressin via Vasopressin Receptor and Gα Proteins Regulations in Cirrhotic Rats

Diabetes Diminishes the Portal-Systemic Collateral Vascular Response to Vasopressin via Vasopressin Receptor and Gα Proteins Regulations in Cirrhotic Rats

Effects of selective double portazygous disconnection and devascularization on hemodynamics of the portal venous system

Vasoactive Substances and Inflammatory Factors in Progression of Liver Cirrhosis with Portal Hypertension

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