AIM To analyze whether there were statistically significant differences in serum sex hormones and renin angiotensin aldosterone system (RAAS) in women with primary hypertension during the reproductive period, the perimenopausal period and the postmenopausal period and to explore the relationship between sex hormones and RAAS in hypertensive women of different ages.
METHODS 207 women with primary hypertension who visited the People’s Hospital of Gansu Province from November 2020 to November 2023 were selected and divided into three groups: reproductive women (Group A, n=51), perimenopausal women (Group B, n=79), and postmenopausal women (Group C, n=77). Compare the estrogen (E2), testosterone (T), prolactin (PRL), follicle stimulating hormone (FSH), luteinizing hormone (LH), dehydroepiandrosterone sulfate (DHEA-S), progesterone (P), and levels of renin (PRA) and aldosterone (ALD) in supine and upright positions among three groups of patients, And the Spearman method was used to analyze the relationship between sex hormones and RAAS in three groups of patients.
RESULTS In reproductive-age women (Group A), perimenopausal women (Group B), and postmenopausal women (Group C), there were significant differences in the hormones E2, FSH, DHEA-S, and P among the three groups (P<0.05), with only Groups A and C showing significant differences in T (P<0.05). LH in Group A was significantly higher than in Groups B and C (P<0.01), and among the three groups, only the standing position Ang II of RAAS showed differences (P<0.05). Spearman correlation analysis showed negative correlations between E2 in Group B and standing PRA, ALD, Ang II, and supine ALD (r=−0.408, P<0.01; r=−0.362, P<0.01; r=−0.278, P<0.01; and r=−0.505, P<0.01), positive correlations between FSH and standing ALD, Ang II, and supine PRA (r=0.316, P<0.01; r=0.344, P<0.01; and r=0.438, P<0.01), positive correlations between LH and standing ALD, Ang II, and supine PRA, ALD (r=0.340, P<0.01; r=0.352, P<0.01; and r=0.439, P<0.01; r=0.374, P<0.05), and negative correlations between P and standing PRA, Ang II, and supine PRA (r=−0.230, P<0.05; r=−0.368, P<0.01; and r=−0.334, P<0.05). In Group C, E2 decreased, while the components of RAAS in the supine and standing positions paradoxically decreased, especially standing Ang II.
CONCLUSION Compared with women with reproductive and postmenopausal hypertension, the levels of RAAS in perimenopausal women are significantly correlated with changes in sex hormones, and the activation of RAAS may be involved in the initiation and progression of hypertension in perimenopausal women.
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