Key result
Angiotensin 1-7 significantly increased skeletal muscle/body weight ratio, fiber cross-sectional area, and twitch and tetanic force in wild-type mice, effects that were absent in MasR-/- mice.
Why the study?
Angiotensin 1-7 prevents skeletal muscle atrophy in disease models, but its hypertrophic effects, impact on contractile function, and reliance on MasR in normal muscle were unknown.
Does Angiotensin 1-7 increase muscle mass and contractile function in juvenile mice?
Does Angiotensin 1-7 increase muscle mass and contractile function in juvenile mice?
Angiotensin 1-7 induces skeletal muscle hypertrophy and increases contractile force in normal juvenile mice via the Mas receptor.
Answers are grounded in this paper and cite their sources.
Juvenile mouse data extend Ang 1-7 muscle effects to developing animals; leaves open translation to human myopathies.
Recent studies reported that in skeletal muscle angiotensin 1–7 (Ang 1–7), via its receptor Mas (MasR), prevents the atrophy induced by angiotensin II and by cast immobilization; it also improves muscle integrity and function in the mdx mouse, a muscular dystrophy model. The objectives of this study were to document 1) the extent of the Ang 1–7’s hypertrophic effect in terms of muscle mass and muscle fiber cross-sectional area (CSA), 2) how Ang 1–7 affects muscle contractile function in terms of twitch and tetanic force, force-frequency relationship, and 3) whether the effect involves MasR. Wild-type and MasR-deficient [Mas receptor knockout mouse model ( MasR −/− )] mice were treated with Ang 1–7 (100 ng/kg body wt·min using an osmotic pump) for 4 or 16 wk. Ang 1–7 significantly increased skeletal muscle/body weight ratio of soleus, tibialis, and gastrocnemius, but not of extensor digitorum longus (EDL). It significantly increased fiber cross-sectional area in the order of type I > IIA > IIB. In EDL and soleus muscles, it significantly increased twitch and tetanic force while causing a shift in the force-frequency relationship toward lower stimulation frequencies. It had no effect on fiber type composition. None of the Ang 1–7 effects observed in wild-type mice were observed in MasR −/− muscles. It caused a transient increase in phosphorylated protein kinase B (Akt) and 4EBP proteins while having no effect on S6 phosphorylation, MuRF-1, and atrogin-1 and a decrease in PAX7 expression in satellite cells. This is the first study demonstrating the hypertrophic effects of Ang 1–7 in normal muscle acting via its MasR.
No takes yet. Share an insight, caveat, or question.
Albadrani et al. (2022) studied Normal muscle. Angiotensin 1-7 vs. MasR-/- mice / untreated was evaluated on Muscle mass, muscle fiber cross-sectional area (CSA), and muscle contractile function. Angiotensin 1-7 significantly increased skeletal muscle/body weight ratio, fiber cross-sectional area, and twitch and tetanic force in wild-type mice, effects that were absent in MasR-/- mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: