What question did this study set out to answer?

To assess the direct vasomotor effects of angiotensin II and determine whether subvasomotor levels impair endothelium-dependent nitric oxide-mediated dilation via superoxide production in coronary microvessels.

February 20, 2003Circulation Research

Divergent Roles of Angiotensin II AT 1 and AT 2 Receptors in Modulating Coronary Microvascular Function

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Why the study?

Does Angiotensin II modulate coronary microvascular function via AT1 and AT2 receptors in isolated porcine coronary arterioles?

Population

Isolated porcine coronary arterioles

Comparison

Angiotensin II at various concentrations, with… vs Control conditions

Design

Preclinical

Authors

CZCuihua ZhangYanshan University THTravis W. HeinTexas A&M Health Science Center WWWei WangZhejiang International Studies University

Discussion

Member takes

Implication

Ang II's concentration-dependent effects in porcine arterioles leave open their role in human coronary microvascular dysfunction; hypothesis-generating for AT1/AT2-targeted interventions.

Key Points

To assess the direct vasomotor effects of angiotensin II and determine whether subvasomotor levels impair endothelium-dependent nitric oxide-mediated dilation via superoxide production in coronary microvessels.
Examined diameter changes in isolated porcine coronary arterioles exposed to varying concentrations of angiotensin II alone and in combination with AT1 (losartan) or AT2 (PD 123319) receptor antagonists.
Assessed endothelium-dependent dilation to adenosine and vascular superoxide production after vessel pretreatment with subvasomotor angiotensin II (0.1 nmol/L for 60 minutes) alongside TEMPOL, apocynin, or L-NMMA.
Angiotensin II induced vasoconstriction at a low concentration (1 nmol/L) via AT1 receptors and vasodilation at higher concentrations (>10 nmol/L) via AT2 receptors.
Pretreatment with subvasomotor angiotensin II (0.1 nmol/L) attenuated adenosine-stimulated nitric oxide production and vasodilation, an effect that was absent after endothelial removal or in the presence of L-NMMA.
Inhibition of dilation and arteriolar superoxide production induced by angiotensin II were abolished by losartan, the superoxide scavenger TEMPOL, and the NADPH oxidase inhibitor apocynin.

Structured PICO

Does Angiotensin II modulate coronary microvascular function via AT1 and AT2 receptors in isolated porcine coronary arterioles?

Population

Isolated porcine coronary arterioles

Intervention

Angiotensin II (Ang II) at various concentrations (1 nmol/L, >10 nmol/L, 0.1 nmol/L), with or without AT1 receptor antagonist losartan, AT2 receptor antagonist PD 123319, L-NMMA, TEMPOL, or apocynin

Comparator

Control conditions (without Ang II or with specific antagonists)

Outcome

Vasomotor action (vasoconstriction/vasodilation) and endothelium-dependent NO-mediated dilationsurrogate

Angiotensin II exerts divergent effects on coronary microvascular function, causing AT1-mediated vasoconstriction and AT2-mediated vasodilation, while subvasomotor levels impair NO-mediated dilation via oxidative stress.

Cite This Study

Zhang et al. (2003) studied this question.

synapsesocial.com/papers/6a70ff53e36a167817e2d3ce https://doi.org/10.1161/01.res.0000056759.53828.2c

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Implication

Ang II's concentration-dependent effects in porcine arterioles leave open their role in human coronary microvascular dysfunction; hypothesis-generating for AT1/AT2-targeted interventions.

Divergent Roles of Angiotensin II AT 1 and AT 2 Receptors in Modulating Coronary Microvascular Function

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Divergent Roles of Angiotensin II AT 1 and AT 2 Receptors in Modulating Coronary Microvascular Function

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider