Key result
The [SII] AngII analogue stimulated beta-arrestin2-dependent ERK1/2 phosphorylation without activating Gq-coupling or inducing inotropic or chronotropic effects in cardiac myocytes and perfused hearts.
Population
Native preparations of cardiac myocytes and Langendorff-perfused beating hearts
Comparison
[Sar, Ile, Ile]-AngII analogue vs Angiotensin II (AngII)
Design
Preclinical
Authors
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Distinguishes beta-arrestin2 from Gq AT1R effects in rodent myocardium; leaves open therapeutic translation to human heart disease.
The AT1R can activate ERK1/2 via G protein-independent, beta-arrestin2-dependent pathways in the heart, leading to distinct subcellular localization and physiological effects compared to G protein-dependent activation.
Aplin et al. (2007) studied this question. [Sar(1), Ile(4), Ile(8)]-AngII ([SII] AngII) analogue vs. Angiotensin II was evaluated on ERK1/2 activation and inotropic/chronotropic effects. The [SII] AngII analogue stimulated beta-arrestin2-dependent ERK1/2 phosphorylation without activating Gq-coupling or inducing inotropic or chronotropic effects in cardiac myocytes and perfused hearts.
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