Key result
Elevated follicle stimulating hormone (FSH) stimulated renin production and increased blood pressure in ovariectomized mice, indicating an estrogen-independent mechanism for post-menopausal hypertension.
Why the study?
Post-menopausal hypertension has been attributed solely to declining estrogen, prompting research into how follicle stimulating hormone increases renin production involved in blood pressure regulation.
Does follicle stimulating hormone promote renin production and increase blood pressure in an ovariectomized mouse model?
Population
Renal juxtaglomerular cells, As4.1 mouse cells, and ovariectomized mice
Comparison
Ovariectomy vs ovariectomy plus GnRHa vs ovariectomy with estrogen and recombinant FSH
Design
Preclinical animal and cell-culture experimental study
Authors
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No immediate clinical implications; leaves open whether FSH drives renin and BP independently of estrogen in women.
Does follicle stimulating hormone promote renin production and increase blood pressure in an ovariectomized mouse model?
p-value: p=<0.05
Elevated FSH stimulates renin production via FSH receptors in renal juxtaglomerular cells, providing a potential estrogen-independent mechanism for post-menopausal hypertension.
Yu et al. (2022) studied Post-menopausal hypertension (n=40). Follicle stimulating hormone (FSH) vs. Sham, OVX alone, or OVX + GnRHa was evaluated on Renin production and blood pressure (SBP, DBP, MAP) (p=<0.05). Elevated follicle stimulating hormone (FSH) stimulated renin production and increased blood pressure in ovariectomized mice, indicating an estrogen-independent mechanism for post-menopausal hypertension.
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