Key result
Chronic high-dose Angiotensin II treatment increased myocardial collagen content from 2.9% to 4.3% and caused marked diastolic dysfunction after ischemia, with no protective effect from female gender.
Why the study?
Does chronic high-dose angiotensin II induce gender-dependent differences in gene expression, remodeling, and ischemia tolerance in rat hearts?
Does chronic high-dose angiotensin II induce gender-dependent differences in gene expression, remodeling, and ischemia tolerance in rat hearts?
Absolute Event Rate: 4.3% vs 2.9%
p-value: p=<0.05
Chronic sub-toxic levels of Ang II induce non-hypertrophic remodeling, fibrosis, and post-ischemic diastolic dysfunction in rat hearts, with no overall protective effect of female gender.
Alerts to Ang II-driven diastolic impairment in rat models; leaves open clinical translation and gender effects in humans.
To examine the response to chronic high-dose angiotensin II (Ang II) and a proposed milder response in female hearts with respect to gene expression and ischemic injury. Female and male litter-matched rats were treated with 400 ng kg(-1) min(-1) Ang II for 14 days. Hearts were isolated, subjected to 30-min ischemia and 30-min reperfusion in combination with functional monitoring and thereafter harvested for gene expression, WB and histology. Ang II-treated hearts showed signs of non-hypertrophic remodeling and had significantly higher end diastolic pressure after reperfusion, but no significant gender difference was detected. Ang II increased expression of genes related to heart function (ANF, β-MCH, Ankrd-1, PKC-α, PKC-δ TNF-α); fibrosis (Col I-α1, Col III-α1, Fn-1, Timp1) and apoptosis (P53, Casp-3) without changing heart weight but with 68% increase in collagen content. High (sub-toxic) dose of Ang II resulted in marked heart remodeling and diastolic dysfunction after ischemia without significant myocyte hypertrophy or ventricular chamber dilatation. Although there were some gender-dependent differences in gene expression, female gender did not protect against the overall response.
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Aljabri et al. (2010) studied Ischemia-reperfusion injury and heart remodeling (n=45). Angiotensin II vs. Sham was evaluated on Collagen content in transverse sections (p=<0.05). Chronic high-dose Angiotensin II treatment increased myocardial collagen content from 2.9% to 4.3% and caused marked diastolic dysfunction after ischemia, with no protective effect from female gender.
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