The Effect of Endogenous Angiotensin II on Alveolar Fluid Clearance in Rats with Acute Lung Injury

Deng, Jia; Wang, Daoxin; Deng, Wang; Li, Changyi; Jin, Tong

doi:10.1155/2012/951025

Cited by 39 publications

(43 citation statements)

References 18 publications

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“…LPS increases the levels of AngII which acts through AT 1 R [79]. Thus the effect of Ang-(1-7) on LPS-induced muscle wasting may be due to the fact that Ang-(1-7) antagonizes the direct effect of AngII on skeletal muscle, as we have demonstrated recently [40,41].…”

Section: Discussionmentioning

confidence: 68%

Endotoxin-induced skeletal muscle wasting is prevented by angiotensin-(1–7) through a p38 MAPK-dependent mechanism

et al. 2015

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Skeletal muscle atrophy induced during sepsis syndrome produced by endotoxin in the form of LPS (lipopolysaccharide), is a pathological condition characterized by the loss of strength and muscle mass, an increase in MHC (myosin heavy chain) degradation, and an increase in the expression of atrogin-1 and MuRF-1 (muscle-specific RING-finger protein 1), two ubiquitin E3 ligases belonging to the ubiquitin-proteasome system. Ang-(1-7) [Angiotensin-(1-7)], through its Mas receptor, has beneficial effects in skeletal muscle. We evaluated in vivo the role of Ang-(1-7) and Mas receptor on the muscle wasting induced by LPS injection into C57BL/10J mice. In vitro studies were performed in murine C2C12 myotubes and isolated myofibres from EDL (extensor digitorum longus) muscle. In addition, the participation of p38 MAPK (mitogen-activated protein kinase) in the Ang-(1-7) effect on the LPS-induced muscle atrophy was evaluated. Our results show that Ang-(1-7) prevents the decrease in the diameter of myofibres and myotubes, the decrease in muscle strength, the diminution in MHC levels and the induction of atrogin-1 and MuRF-1 expression, all of which are induced by LPS. These effects were reversed by using A779, a Mas antagonist. Ang-(1-7) exerts these anti-atrophic effects at least in part by inhibiting the LPS-dependent activation of p38 MAPK both in vitro and in vivo. We have demonstrated for the first time that Ang-(1-7) counteracts the skeletal muscle atrophy induced by endotoxin through a mechanism dependent on the Mas receptor that involves a decrease in p38 MAPK phosphorylation. The present study indicates that Ang-(1-7) is a novel molecule with a potential therapeutic use to improve muscle wasting during endotoxin-induced sepsis syndrome.

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Section: Discussionmentioning

confidence: 68%

Endotoxin-induced skeletal muscle wasting is prevented by angiotensin-(1–7) through a p38 MAPK-dependent mechanism

et al. 2015

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“…Studies have shown that Ang II as an important component of RAS is involved in the pathogenesis of lung injury in different models, and most actions of Ang II are related to the AT1 receptor. Thus, strategies that aim to inhibit Ang II production and/or its receptor have been found to exert protective effects [11,12]. Deng et al [11] found endogenous that Ang II could inhibit alveolar fluid clearance and dysregulate α‐epithelial sodium channel expression via AT1 receptors, which contributed to the alveolar filling and pulmonary edema in lipopolysaccharide‐induced ALI [11].…”

Section: Discussionmentioning

confidence: 99%

“…Thus, strategies that aim to inhibit Ang II production and/or its receptor have been found to exert protective effects [11,12]. Deng et al [11] found endogenous that Ang II could inhibit alveolar fluid clearance and dysregulate α‐epithelial sodium channel expression via AT1 receptors, which contributed to the alveolar filling and pulmonary edema in lipopolysaccharide‐induced ALI [11]. In radiation‐induced lung injury, Ang II significantly increased in the lung even at 6 months after irradiation [12].…”

Section: Discussionmentioning

confidence: 99%

Captopril pretreatment protects the lung against severe acute pancreatitis induced injury via inhibiting angiotensin II production and suppressing Rho/ROCK pathway

Guo

Cao

et al. 2016

The Kaohsiung J of Med Scie

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Acute pancreatitis (AP) usually causes acute lung injury, which is also known as acute pancreatitis associated lung injury (APALI). This study aimed to investigate whether captopril pretreatment was able to protect lung against APALI via inhibiting angiotensin II (Ang II) production and suppressing Rho/ROCK (Rho kinase) pathway in rats. Severe AP (SAP) was introduced to rats by bile-pancreatic duct retrograde injection of 5% sodium taurocholate. Rats were randomly divided into three groups. In the sham group, sham operation was performed; in the SAP group, SAP was introduced; in the pre-cpl + SAP group, rats were intragastrically injected with 5 mg/kg captopril 1 hour prior to SAP induction. Pathological examination of the lung and pancreas, evaluation of pulmonary vascular permeability by wet/dry ratio and Evans Blue staining, detection of serum amylase, Western blot assay for Ang II receptor type 1 (AT1), RhoA, ROCK (Rho kinase), and MLCK (myosin light chain kinase) were performed after the animals were sacrificed at 24 hours. After the surgery, characteristic findings of pancreatitis were observed, accompanied by lung injury. The serum amylase, Ang II, and lung expression of AT1, RhoA, ROCK, and MLCK increased dramatically in SAP rats. However, captopril pretreatment improved the histological changes, reduced the pathological score of the pancreas and lung, inhibited serum amylase and Ang II production, and decreased expression of AT1, RhoA, ROCK, and MLCK in the lung. These findings suggest that captopril pretreatment is able to protect the lung against APALI, which is, at least partially, related to the inhibition of Ang II production and the suppression of the Rho/ROCK pathway.

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“…Na, K‐ATPase plays the role of sodium pump that works in concert with apical ENaC in regulating AFC . A 2 B adenosine receptor agonists, angiotensin, tri‐Iodo‐L‐thyronine and oestradiol have exhibited increasing AFC effects via promoting ENaC or Na, K‐ATPase activity in animal studies . However, these studies remain unsuccessful in humans .…”

Section: Introductionmentioning

confidence: 99%

“…A 2 B adenosine receptor agonists, angiotensin, tri‐Iodo‐L‐thyronine and oestradiol have exhibited increasing AFC effects via promoting ENaC or Na, K‐ATPase activity in animal studies . However, these studies remain unsuccessful in humans . Previously, we reported that administration of a β‐agonist salbutamol (iv) decreased extravascular pulmonary fluid in ALI/ARDS patients.…”

Section: Introductionmentioning

confidence: 99%

Maresin Conjugates in Tissue Regeneration 1 improves alveolar fluid clearance by up‐regulating alveolar ENaC, Na, K‐ATPase in lipopolysaccharide‐induced acute lung injury

Han

Bhandari

et al. 2020

J Cellular Molecular Medi

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Maresin Conjugates in Tissue Regeneration 1 (MCTR1) is a newly identified macrophage-derived sulfido-conjugated mediator that stimulates the resolution of inflammation. This study assessed the role of MCTR1 in alveolar fluid clearance (AFC) in a rat model of acute lung injury (ALI) induced by lipopolysaccharide (LPS). Rats were intravenously injected with MCTR1 at a dose of 200 ng/rat, 8 hours after administration of 14 mg/kg LPS. The level of AFC was then determined in live rats.Primary rat ATII (Alveolar Type II) epithelial cells were also treated with MCTR1 (100 nmol/L) in a culture medium containing LPS for 8 hours. MCTR1 treatment improved AFC (18.85 ± 2.07 vs 10.11 ± 1.08, P < .0001) and ameliorated ALI in rats.MCTR1 also significantly promoted AFC by up-regulating epithelial sodium channel (ENaC) and Na + -K + -adenosine triphosphatase (Na, K-ATPase) expressions in vivo.MCTR1 also activated Na, K-ATPase and elevated phosphorylated-Akt (P-Akt) by up-regulating the expression of phosphorylated Nedd4-2 (P-Nedd4-2) in vivo and in vitro. However, BOC-2 (ALX inhibitor), KH7 (cAMP inhibitor) and LY294002 (PI3K inhibitor) abrogated the improved AFC induced by MCTR1. Based on the findings of this study, MCTR1 may be a novel therapeutic approach to improve reabsorption of pulmonary oedema during ALI/acute respiratory distress syndrome (ARDS). K E Y W O R D SALI/ARDS, alveolar fluid clearance, ENaC, MCTR1, Na, K-ATPase | 4737 HAN et Al.

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The Effect of Endogenous Angiotensin II on Alveolar Fluid Clearance in Rats with Acute Lung Injury

Abstract: These findings suggest that endogenous Ang II inhibits AFC and dysregulates ENaC expression via AT1 receptors, which contribute to alveolar filling and pulmonary edema in LPS-induced ALI.

Cited by 39 publications

References 18 publications

Endotoxin-induced skeletal muscle wasting is prevented by angiotensin-(1–7) through a p38 MAPK-dependent mechanism

Endotoxin-induced skeletal muscle wasting is prevented by angiotensin-(1–7) through a p38 MAPK-dependent mechanism

Captopril pretreatment protects the lung against severe acute pancreatitis induced injury via inhibiting angiotensin II production and suppressing Rho/ROCK pathway

Maresin Conjugates in Tissue Regeneration 1 improves alveolar fluid clearance by up‐regulating alveolar ENaC, Na, K‐ATPase in lipopolysaccharide‐induced acute lung injury

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