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Postmenopausal response to angiotensin II‐induced hypertension is blunted during perimenopause: a study in the accelerated ovarian failure (AOF) model of menopause
Author(s) -
Pollow Dennis,
Perez Jessica,
Booth Allyson,
Constantopoulos Eleni,
Konhilas John P,
Brooks Heddwen L
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1112.3
Subject(s) - menopause , medicine , endocrinology , angiotensin ii , blood pressure
A female's risk of developing hypertension (HTN) increases dramatically after menopause. This study aimed to investigate the onset of ANG II‐induced HTN in the AOF model of menopause (VCD model). The AOF model preserves a perimenopausal period in mice, which is increasingly recognized as a critical timeframe for the treatment and prevention of diseases. We hypothesized that ANG II‐infusion would elicit a differential response when administered in peri vs postmenopause and examined the cardiovascular and renal impact. Female VCD treated BL/6 mice (peri and postmenopause) received 800 ng/kg/min ANG II via osmotic mini‐pump for 10 days. ANG II elicited a significant increase in MAP in postmenopausal females (ANG/POST) vs cycling females (C 105 vs ANG 128 vs ANG/POST 143 mmHg, P<0.05). In contrast, there was no difference in MAP in the perimenopause study; ANG II increased MAP in cycling and PERI groups (~126 mmHg). AQP2 protein expression significantly decreased in the renal cortex of ANG/POST mice alone (C 100 vs ANG 98 vs ANG/POST 78%). Renal inflammation, measured by ICAM‐1and F4/80 staining, increased in ANG/POST vs all other groups. Cardiac collagen volume fraction significantly increased in ANG/POST vs ANG (C 0.36 vs ANG 1.36 vs ANG/POST 2.94%). Our data suggests that the perimenopause to menopause transition is a key stage in the loss of a female's protection against developing HTN, and renal and CV complications.