April 3, 2019Bioscience ReportsOpen Access

AngA infusion at 10 μg/kg/min led to abdominal aortic dilation in 3 of 10 mice with no rupture, whereas a 10-fold lower rate of AngII (1 μg/kg/min) led to dilation or rupture in 8 of 10 mice.

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Why the study?

It was unknown whether the single amino acid change decarboxylating the N-terminal residue of AngII to form AngA impacts AngII effects on abdominal aortic aneurysm formation.

Does Angiotensin A induce abdominal aortic aneurysm formation similarly to Angiotensin II in Ldlr or Apoe deficient mice?

Population

Male Ldlr or Apoe deficient mice

Comparison

AngA infusion vs AngII infusion vs co-infusion

Design

Preclinical animal study with computational analyses

Follow-up

4 weeks

Authors

WYWang Ya YXYinchuan Xu CWCongqing Wu

Discussion

Member takes

Overview

AngA may not model AngII-driven AAA in mice; leaves open whether the N-terminal residue drives human aneurysm pathogenesis.

Structured PICO

Does Angiotensin A induce abdominal aortic aneurysm formation similarly to Angiotensin II in Ldlr or Apoe deficient mice?

Population

Male low-density lipoprotein receptor (Ldlr) or apolipoprotein E (Apoe) deficient mice

Intervention

Angiotensin A (AngA) infusion (1 μg/kg/min or 10 μg/kg/min) for 4 weeks

Comparator

Angiotensin II (AngII) infusion (1 μg/kg/min) for 4 weeks

Outcome

Abdominal aortic aneurysm (AAA) formation (aortic dilation or rupture)surrogate

Angiotensin A has significantly diminished effects on abdominal aortic aneurysm formation compared to Angiotensin II, highlighting the pathophysiological importance of the first amino acid of AngII.

Cite This Study

Ya et al. (2019) studied this question.

synapsesocial.com/papers/6a821bc4e282fcaf79c69ed8 https://doi.org/10.1042/bsr20182055

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April 3, 2019Bioscience ReportsOpen Access

AngA infusion at 10 μg/kg/min led to abdominal aortic dilation in 3 of 10 mice with no rupture, whereas a 10-fold lower rate of AngII (1 μg/kg/min) led to dilation or rupture in 8 of 10 mice.

View Full Paper

Ask AI

Bookmark

Why the study?

It was unknown whether the single amino acid change decarboxylating the N-terminal residue of AngII to form AngA impacts AngII effects on abdominal aortic aneurysm formation.

Does Angiotensin A induce abdominal aortic aneurysm formation similarly to Angiotensin II in Ldlr or Apoe deficient mice?

Population

Male Ldlr or Apoe deficient mice

Comparison

AngA infusion vs AngII infusion vs co-infusion

Design

Preclinical animal study with computational analyses

Follow-up

4 weeks

Authors

WYWang Ya YXYinchuan Xu CWCongqing Wu

Discussion

Member takes

Overview

AngA may not model AngII-driven AAA in mice; leaves open whether the N-terminal residue drives human aneurysm pathogenesis.

Structured PICO

Does Angiotensin A induce abdominal aortic aneurysm formation similarly to Angiotensin II in Ldlr or Apoe deficient mice?

Population

Male low-density lipoprotein receptor (Ldlr) or apolipoprotein E (Apoe) deficient mice

Intervention

Angiotensin A (AngA) infusion (1 μg/kg/min or 10 μg/kg/min) for 4 weeks

Comparator

Angiotensin II (AngII) infusion (1 μg/kg/min) for 4 weeks

Outcome

Abdominal aortic aneurysm (AAA) formation (aortic dilation or rupture)surrogate

Angiotensin A has significantly diminished effects on abdominal aortic aneurysm formation compared to Angiotensin II, highlighting the pathophysiological importance of the first amino acid of AngII.

Cite This Study

Ya et al. (2019) studied this question.

synapsesocial.com/papers/6a821bc4e282fcaf79c69ed8 https://doi.org/10.1042/bsr20182055

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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