Angiotensin II-Induced Pulmonary Edema in a Rabbit Model.

Yamamoto, Takatsugu; Wang, Liman; Shimakura, Kazuro; Sanaka, Masaki; Koike, Yuichi; Mineshita, Satoru

doi:10.1254/jjp.73.33

Cited by 33 publications

(22 citation statements)

References 14 publications

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“…By equalizing the dose of losartan and EXP3174 to 0.4 mg/kg, the duration of action was longer, an observation which is consistent with previous reports. 35 As was expected 0.4 mg/kg of losartan compared with 0.2 mg/kg resulted in further reduction of the maximum blood pressure response to Ang II infusion.…”

Section: Discussionsupporting

confidence: 52%

Hypertension study in anaesthetized rabbits: protocol proposal for AT₁ antagonists screening

Politi

Zervou

Triantafyllidi

et al. 2010

J Renin Angiotensin Aldosterone Syst

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Introduction: The aim of this study was to establish an optimized fast and safe protocol for the pharmacological screening of AT 1 antagonists. Materials and methods: The pharmaceutical prototype AT 1 antagonist losartan, its active metabolite EXP3174 and the synthetic compound MMK1 were analysed in order to validate the protocol. Ang II was continuously infused while the animals received the drugs in two procedures. Results: In the post-treatment procedure drugs were administered either in a single bolus dose or in a sequential manner. When losartan was administered in a single bolus dose, efficacy was evident until the 7th min (p=0.012) whilst EXP3174 infusion extended the efficiency up to the end of the study (p=0.006). In addition, the sequential injections of losartan prolonged the inhibitory time interval until the end of the study (p=0.045). In the pre-treatment procedure, results suggested a dosedependent inhibitory effect for both antagonists. The pressor response to Ang II was unchanged after MMK1 administration either in the post-or in the pre-treatment mode. Conclusions:The proposed protocol appears to be safe, simple and fast for the pharmacological screening of AT 1 antagonists and enables the evaluation of new antagonists using lower doses than any other reported in the literature.

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Section: Discussionsupporting

confidence: 52%

Hypertension study in anaesthetized rabbits: protocol proposal for AT₁ antagonists screening

Politi

Zervou

Triantafyllidi

et al. 2010

J Renin Angiotensin Aldosterone Syst

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“…Associations between the D allele and the development or progression of sarcoidosis [26], asthma [27] and berylliosis [28] have been described. Due to the influence of the pulmonary RAS on vascular permeability [3], vascular tone [4], fibroblast activity [5] and alveolar epithelial cell survival [6], its strong effect upon the natural course of ARDS is comprehensible. Within the lung, the pulmonary circulation is a potentially important site of RAS activation.…”

Section: Discussionmentioning

confidence: 99%

“…ACE inhibitors attenuate pulmonary vasoconstriction in healthy humans and in patients with cor pulmonale [4], as do type-1 AT receptor antagonists [29]. Infusion of AT-I [30] or AT-II [3] can evoke pulmonary oedema independently of catecholamine release. AT-II may, therefore, also affect microvascular permeability.…”

Section: Discussionmentioning

confidence: 99%

“…The early stages of ARDS are characterised by a high permeability pulmonary oedema, alveolar epithelial cell loss and neutrophil infiltration, which may progress to significant alveolar and interstitial remodelling and fibrosis. Experimental evidence suggests that activation of the pulmonary renin-angiotensin system (RAS) may influence the pathogenesis of ARDS via mechanisms affecting vascular permeability [3], vascular tone [4], fibroblast proliferation [5] and by decreasing alveolar epithelial cell survival [6].…”

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confidence: 99%

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ACE I/D but not AGT (-6)A/G polymorphism is a risk factor for mortality in ARDS

Adamzik

Frey²,

Sixt³

et al. 2007

European Respiratory Journal

101

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The intrapulmonary renin-angiotensin system via tissue concentration of angiotensin II or bradykinin may have multiple effects on pulmonary pathophysiology. Therefore, it was investigated whether the presence of the D allele of the angiotensinconverting enzyme (ACE) insertion/deletion (I/D) polymorphism or the A allele of angiotensinogen (AGT) promoter polymorphism (-6)A/G are independent risk factors for 30-day survival in acute respiratory distress syndrome (ARDS) patients.In a prospective study, adults (Germans of Caucasian ethnicity) with ARDS (n584) were recruited from the current authors' intensive care unit and genotyped for the ACE I/D and the AGT (-6)A/G polymorphisms, as were 200 healthy Caucasian controls.Mortality was increased in the ACE DD genotype compared with the I allele, and the ACE I/D polymorphism was an independent prognostic factor for 30-day survival. Patients with a homozygous DD genotype were at highest risk for death (hazard ratio 5.7; 95% confidence interval 1.7-19.2) compared with the II genotype. In contrast, the AGT (-6)A/G polymorphism was neither associated with an increased risk for development of ARDS nor with outcome.In patients with acute respiratory distress syndrome, the angiotensin-converting enzyme insertion/deletion polymorphism but not the angiotensinogen (-6)A/G promoter polymorphism is an independent risk factor with a pronounced effect on 30-day survival.

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“…Rigat et al found that plasma ACE levels of subjects who carried the DD genotype were twofold compared to levels found in patients carrying the II genetic polymorphism (ID subjects having intermediate levels). 22 Previous studies suggested that the activation of the renin-angiotensin system in the lung may be related to the development of ARDS, probably because of decreased alveolar epithelial cell survival, 5 changes in vascular permeability 23 or fibroblast proliferation. 24 ACE levels were elevated in BAL and administration of ACEI protected the rats from severe lungs injury.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme I/D polymorphism and acute respiratory distress syndrome

Deng

Zhang

Jin

et al. 2015

J Renin Angiotensin Aldosterone Syst

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Background: Some studies have assessed the association between angiotensin-converting enzyme (ACE) I/D polymorphism and acute respiratory distress syndrome (ARDS) risk. However, the results have been inconclusive and contradictory. Therefore, we performed a meta-analysis to investigate the association between ACE I/D polymorphism and ARDS risk. Methods: All relevant studies were searched using PubMed and EMBASE. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated using random-effects models or fixed-effects models. Results: A total of 14 studies with 5218 subjects were included in this meta-analysis. We found that ACE I/D polymorphism significantly associated with an increased ARDS risk (OR=1.57; 95% CI 1.30–1.89; P<0.00001). In the subgroup analysis by race, Caucasians with ACE I/D polymorphism showed increased ARDS risk (OR=1.63; 95% CI 1.32–2.02; P<0.00001). However, Asians with this polymorphism did not show significantly increased ARDS risk (OR=1.31; 95% CI 0.90–1.90; P=0.95). In the subgroup analysis by age group, adults showed increased ARDS risk (OR=1.60; 95% CI 1.32–1.93; P<0.00001), while pediatric patients did not have increased ARDS risk (OR=1.15; 95% CI 0.57–2.30; P=0.70). Conclusions: This meta-analysis suggested that ACE I/D polymorphism might contribute to the susceptibility for ARDS.

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Angiotensin II-Induced Pulmonary Edema in a Rabbit Model.

Cited by 33 publications

References 14 publications

Hypertension study in anaesthetized rabbits: protocol proposal for AT₁ antagonists screening

Hypertension study in anaesthetized rabbits: protocol proposal for AT₁ antagonists screening

ACE I/D but not AGT (-6)A/G polymorphism is a risk factor for mortality in ARDS

Angiotensin-converting enzyme I/D polymorphism and acute respiratory distress syndrome

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Angiotensin II-Induced Pulmonary Edema in a Rabbit Model.

Cited by 33 publications

References 14 publications

Hypertension study in anaesthetized rabbits: protocol proposal for AT1 antagonists screening

Hypertension study in anaesthetized rabbits: protocol proposal for AT1 antagonists screening

ACE I/D but not AGT (-6)A/G polymorphism is a risk factor for mortality in ARDS

Angiotensin-converting enzyme I/D polymorphism and acute respiratory distress syndrome

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Hypertension study in anaesthetized rabbits: protocol proposal for AT₁ antagonists screening

Hypertension study in anaesthetized rabbits: protocol proposal for AT₁ antagonists screening