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Pregnant rats treated with a high fat/pro‐oxidant western diet with angiotensin II and tumor necrosis factor α are resistant to elevations in blood pressure (BP) and have the normal fall in BP during late pregnancy (1084.1)
Author(s) -
Cunningham Mark,
West Crystal,
Baylis Chris
Publication year - 2014
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.28.1_supplement.1084.1
Subject(s) - medicine , saline , endocrinology , angiotensin ii , blood pressure , tumor necrosis factor alpha , oxidative stress
Increased oxidative stress and inflammation are risk factors for hypertension in pregnancy. Here we examined the systolic BP (SBP) via telemetry in virgin (V) and pregnant (P) rats treated with a HFD, ANG II, and TNFα. Methods: Female Sprague Dawley rats were pretreated with a normal diet (ND) or a HFD for 8 weeks before mating. Day 6 P and age‐matched V rats were implanted with either a mini‐pump infusion of saline or ANGII (150 ng/kg/min) + TNFα (75ng/day) for 14 days and sacrificed at gestational day 21. Groups consisted of: V Con (ND + Saline, n=7); V Treatment (HFD + ANGII/TNFα, n=7); P Con (ND + Saline, n=6); P Treatment (HFD + ANGII/TNFα, n=8). Results: The total pressor response (area under the curve [AUC]) increased in V Treatment rats compared to V Con rats (AUC: 120±32 vs. ‐35±29 mmHg X 20 days, P< 0.05) and in P Treatment rats compared to P Con rats (AUC: 61±28 vs. 21±30 mmHg X 20 days, P< 0.05). However the pressor response was greater in V Treatment rats vs. P Treatment rats (120±32 vs. 21±30 mmHg X 20 days, P< 0.05). Both treated and untreated P rats had a normal decrease in SBP at day 20 of pregnancy. Conclusion: Pregnant rats subjected to chronic HFD + pro‐oxidant and pro‐inflammatory insults have a blunted pressor response compared to V Treatment rats. P Treatment rats also display the normal decrease in SBP at late pregnancy. Ongoing studies are investigating the mechanism by which the pregnancy milieu is protective.