Key result
Adrenomedullin heterozygote knockout mice exhibited significantly more severe cardiac hypertrophy (intraventricular septum thickness 1.16 mm vs 1.06 mm) and renal dysfunction after Angiotensin II infusion compared to wild-type mice.
Why the study?
Does endogenous adrenomedullin deficiency exacerbate angiotensin II-induced cardiac hypertrophy and renal damage in mice?
Population
80 12-week-old male mice, comprising 42 wild-type and 38 adrenomedullin heterozygote knockout mice.
Comparison
Angiotensin II infusion in AM+/- mice. vs Angiotensin II infusion in wild-type mice.
Design
Preclinical, Histological analysis evaluated under blind conditions
Follow-up
14 days
Authors
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Supports protective role of endogenous adrenomedullin against Ang II injury; hypothesis-generating for human therapeutic applications.
Does endogenous adrenomedullin deficiency exacerbate angiotensin II-induced cardiac hypertrophy and renal damage in mice?
Absolute Event Rate: 1.16% vs 1.06%
p-value: p=<0.01
Endogenous adrenomedullin plays a critical protective role against angiotensin II-induced cardiac hypertrophy and renal dysfunction in a mouse model.
Niu et al. (2003) studied Cardiac hypertrophy and renal damage (n=80). Adrenomedullin heterozygote knockout (AM+/-) vs. Wild-type (AM+/+) was evaluated on Intraventricular septum thickness (IVST) after 14 days of Angiotensin II infusion (p=<0.01). Adrenomedullin heterozygote knockout mice exhibited significantly more severe cardiac hypertrophy (intraventricular septum thickness 1.16 mm vs 1.06 mm) and renal dysfunction after Angiotensin II infusion compared to wild-type mice.
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