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January 1, 1999Methods and Findings in Experimental and Clinical Pharmacology

Angiotensin II stimulates collagen synthesis via AT1 receptors, while ACE inhibitors and AT1 antagonists reduce myocardial collagen deposition in animal models.

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Why the study?

Does antagonism of the renin-angiotensin-aldosterone system reduce collagen synthesis and deposition in cardiac fibroblasts and myocardium?

Population

Cardiac fibroblasts and rat models including spontaneously hypertensive rats and post-myocardial infarction…

Design

Review

Key result

Angiotensin II stimulates collagen synthesis via AT1 receptors, while ACE inhibitors and AT1 antagonists reduce myocardial collagen deposition in animal models.

Authors

PLPaul LijnenВПВ. А. Петров

Discussion

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Member takes

Overview

Informs antifibrotic strategies targeting RAAS; leaves open translation from animal models to human outcomes.

Structured PICO

Does antagonism of the renin-angiotensin-aldosterone system reduce collagen synthesis and deposition in cardiac fibroblasts and myocardium?

P
Population
Cardiac fibroblasts (in vitro) and rat models including spontaneously hypertensive rats and post-myocardial infarction rats (in vivo)
I
Intervention
Renin-angiotensin-aldosterone system antagonism (ACE inhibitors and AT1 receptor antagonists)
O
Outcome
Collagen synthesis and depositionsurrogate

RAAS antagonism, specifically via ACE inhibitors and AT1 receptor blockers, reduces angiotensin II-mediated collagen synthesis and myocardial fibrosis.

Cite This Study

Lijnen et al. (1999) conducted a review in Myocardial fibrosis. ACE inhibitors and AT1 receptor antagonists was evaluated. Angiotensin II stimulates collagen synthesis via AT1 receptors, while ACE inhibitors and AT1 antagonists reduce myocardial collagen deposition in animal models.

synapsesocial.com/papers/6a0eed8f9df4132b62f9d039https://doi.org/10.1358/mf.1999.21.3.534832
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