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The Kinetics of Angiotensin-I Metabolism in Human Carotid Atheroma: An Emerging Role for Angiotensin (1–7)

Nehmea et al., Vascular Pharmacology (2016) – PMID: 27497910

Product(s) used in this publication:  SpikeTides™ - Proteomics Peptide Standards

Abstract:

AIM:

Local levels of angiotensin peptides depend on their rates of production and degradation, which induce proatherogenic or atheroprotective effects. Here, we reveal the kinetics of Angiotensin-I metabolism in paired early and advanced atherosclerotic lesions.

METHODS:

Lesions were spiked with labeled Ang-I* and supernatants withdrawn after 0, 10, 20, 40 and 80min. The concentration of produced Ang-II*, Ang-III*, Ang-IV* and Ang-(1-7)* peptides were measured using multiple reaction monitoring mass spectrometry coupled to ultra-performance liquid chromatography, normalized to tissue weight and initial [Ang-I*].

RESULTS:

Ang-(1-7)* was the major angiotensin peptide produced, showing increased levels in both tissue types, with 2-3 fold lower levels in advanced compared to early lesions. In contrast, Ang-II* was 2-3 fold higher in advanced compared to early lesions, showing a decrease between 0 and 40min then an increase at 80min in both tissue types. The levels of Ang-IV were stable in both tissue types across all time points. Finally, Ang-III was non-detectable in both lesions across all time points.

CONCLUSION:

Our results suggest that progression of atherosclerosis depends on the increased levels of Ang-II along with the decreased levels of Ang-(1-7), which supports the use of Ang-(1-7) along with Angiotensin type-1 receptor (AT1R) blockers.

Copyright © 2016 Elsevier Inc. All rights reserved.

KEYWORDS:

Angiotensin; Atherosclerosis; Mass spectrometry; Metabolism; Renin-angiotensin-aldosterone system

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