Key result
Transient ACEi attenuates Ang II-induced cardiac fibrosis in spontaneously hypertensive rats via sex-dependent mechanisms.
Why the study?
Prior work showed transient ACEi treatment induced persistent protection against a future stimulus in males, but whether female spontaneously hypertensive rats were responsive was unknown.
Does transient ACEi treatment prevent Ang II-induced cardiac fibrosis in male and female spontaneously hypertensive rats?
Does transient ACEi treatment prevent Ang II-induced cardiac fibrosis in male and female spontaneously hypertensive rats?
Transient ACEi treatment attenuates Ang II-induced cardiac fibrosis in both male and female spontaneously hypertensive rats, but the mechanisms regulating collagen deposition are sex-dependent.
Supports sex-specific antifibrotic effects in hypertensive models; hypothesis-generating and should not yet change practice.
Here, we determine, for the first time that female spontaneously hypertensive rats are responsive to transient angiotensin-converting enzyme inhibitor (ACEi) treatment. Prior work showed that transient ACEi treatment induced persistent protection against a future stimulus in males. Here, Ang II-induced cardiac fibrosis was attenuated by transient ACEi treatment in both sexes. Notably, the underlying mechanism of action is sex-dependent. Specifically, changes in collagen deposition in male but not female hearts correlate with collagen gene expression.
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Garvin et al. (2025) studied Angiotensin II-induced cardiac remodeling. Transient angiotensin-converting enzyme inhibitor (ACEi) was evaluated on Angiotensin II-induced cardiac fibrosis. Transient angiotensin-converting enzyme inhibitor treatment attenuated Ang II-induced cardiac fibrosis in both male and female spontaneously hypertensive rats through sex-dependent mechanisms.
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