Mice modeling menopause show distinct blood pressure signaling
In experiments, male mice and females modeling postmenopause developed similar high blood pressure after 14 days of hormone infusion, but differed in associated brain signaling.
Our read
Mechanisms- Studied:
- Experiments in female mice modeling menopause and age-matched males, 14 days
- What changed:
- Estrogen-receptor activation blocked rising blood pressure in menopause-model mice, but not males
- The catch:
- Only 9 vehicle-treated and 10 agonist-treated menopause-model mice supported the blood pressure comparison
- In the record:
- One of 3 papers on estrogen receptor beta agonists on record: none yet with results in people, 3 in animals.
Editor of record: Boris Djordjevic · AgingResearch.News
Female mice with chemically induced ovarian failure that modeled postmenopause and male mice developed similar high blood pressure in an animal experiment. The researchers infused angiotensin II, a hormone that raises blood pressure, for 14 days.
Recordings from brain slices linked the females’ hypertension to stronger electrical currents through GluA1, part of a receptor that helps nerve cells receive excitatory signals. Another receptor type showed no such increase. The heightened currents appeared to involve GPER1, an estrogen receptor, working with AKAP150, a protein that holds signaling proteins together. Heightened currents in males also depended on AKAP150, but involved a different signaling route.
Why it matters
The authors suggest that high blood pressure at early and late ovarian failure is associated with distinct brain-signaling pathways, pointing to differences across the menopausal transition.
Caveats
The model induced ovarian failure chemically without aging, and researchers measured nerve-cell currents in brain slices. These mouse results do not establish whether the same pathways operate after natural menopause in women.
The paper
Weill Cornell Medicine
Biology of Sex Differences, May 23, 2026, Open access
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