Key result
Angiotensin-(1-7) significantly attenuated the Angiotensin II-mediated increase in myocyte cross-sectional area and interstitial fibrosis, associated with upregulation of dual-specificity phosphatase 1.
Why the study?
Does ANG-(1-7) attenuate ANG II-induced cardiac remodeling in a rat model of hypertension?
Population
Male Sprague-Dawley rats weighing 270-300 g (n=24)
Comparison
ANG- 24 µg·kg⁻¹·h⁻¹ co-infused with ANG II 24… vs ANG II 24 µg·kg⁻¹·h⁻¹ alone via subcutaneous…
Design
Preclinical, Outcome assessors blinded for quantification of myocyte…
Follow-up
4 weeks
Authors
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Does not inform clinical practice; leaves open DUSP-1 as target in human hypertensive remodeling.
Does ANG-(1-7) attenuate ANG II-induced cardiac remodeling in a rat model of hypertension?
Absolute Event Rate: 25.5% vs 57.2%
p-value: p=<0.001
ANG-(1-7) attenuates ANG II-induced cardiac hypertrophy and fibrosis in vivo independently of blood pressure, likely via upregulation of DUSP-1 and subsequent reduction in ERK1/2 activity.
McCollum et al. (2011) studied Angiotensin II-induced cardiac remodeling (n=24). Angiotensin-(1-7) vs. Angiotensin II alone was evaluated on Myocyte cross-sectional area (MCSA) increase compared to saline control (p=<0.001). Angiotensin-(1-7) significantly attenuated the Angiotensin II-mediated increase in myocyte cross-sectional area and interstitial fibrosis, associated with upregulation of dual-specificity phosphatase 1.
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