What question did this study set out to answer?

To determine angiotensin II receptor binding and its relationship to angiotensin converting enzyme (ACE) binding and fibrous tissue formation in damaged rat hearts.

November 1, 1994Cardiovascular Research

Angiotensin II receptor binding following myocardial infarction in the rat

Q: What is the clinical evidence from this study?

Population: Myocardial infarction and tissue repair. Intervention: Lisinopril vs. Sham operated, unoperated controls, infarcted rats without lisinopril. Primary outcome: Angiotensin II receptor and ACE binding densities, and fibrous tissue formation.

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Key result

Increased AT1 receptor binding density is associated with ACE binding and fibrillar collagen formation at sites of fibrous tissue formation following myocardial infarction in rats.

Why the study?

Does lisinopril alter angiotensin II receptor binding and fibrous tissue formation in a rat model of myocardial infarction?

Key Points

To determine angiotensin II receptor binding and its relationship to angiotensin converting enzyme (ACE) binding and fibrous tissue formation in damaged rat hearts.
Assigned rats to five groups: unoperated controls, sham-operated controls, sham plus lisinopril (20 mg/kg/day), coronary artery ligation (myocardial infarction), and infarction plus lisinopril.
Measured angiotensin II receptor and ACE binding densities across hearts harvested at day 3 and weeks 1, 2, 4, and 8 using quantitative in vitro autoradiography.
Identified receptor subtypes by competing radioligand binding with an AT1 antagonist (DuP753/losartan) and an AT2 antagonist (PD123177).
Angiotensin II receptor binding was low in normal myocardium but markedly increased at sites of left ventricular infarction, endocardial fibrosis, pericardiotomy, and suture insertion at all timepoints.
Receptor binding in both normal and connective tissues was completely displaced by the AT1 antagonist DuP753 but unaffected by the AT2 antagonist PD123177.
Lisinopril treatment successfully inhibited ACE and significantly reduced pericardial collagen formation in sham controls, but did not alter AT1 receptor binding density at sites of fibrosis.

Structured PICO

Does lisinopril alter angiotensin II receptor binding and fibrous tissue formation in a rat model of myocardial infarction?

Population

Rat model of tissue repair (pericardiotomy and myocardial infarction with left coronary artery ligation) including 5 groups: sham operated, myocardial infarction, myocardial infarction with lisinopril, sham operated with lisinopril, and unoperated controls.

Intervention

Lisinopril (20 mg.kg-1.d-1 in drinking water)

Comparator

Untreated rats (sham operated, myocardial infarction, or unoperated controls)

Outcome

Angiotensin II receptor binding density, ACE binding density, and fibrous tissue formationsurrogate

In a rat model of myocardial infarction, increased AT1 receptor binding is associated with ACE binding and fibrosis, suggesting AT1 receptors mediate the fibrogenic response to tissue injury.

Discussion

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Implication

Hypothesis-generating for AT1-mediated post-MI fibrosis in rats; leaves open translation to human therapy.

Cite This Study

Sun et al. (1994) studied Myocardial infarction and tissue repair. Lisinopril vs. Sham operated, unoperated controls, infarcted rats without lisinopril was evaluated on Angiotensin II receptor and ACE binding densities, and fibrous tissue formation. Increased AT1 receptor binding density is associated with ACE binding and fibrillar collagen formation at sites of fibrous tissue formation following myocardial infarction in rats.

synapsesocial.com/papers/6a153d4e98b62c6f539f4d29 https://doi.org/10.1093/cvr/28.11.1623

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Angiotensin II receptor binding following myocardial infarction in the rat

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Angiotensin II receptor binding following myocardial infarction in the rat

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider