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Sex differences in a rat model of fetal programming of hypertension
Author(s) -
Ojeda Norma B,
Grigore Daniela,
Roberston Elliott B,
Alexander Barbara T
Publication year - 2006
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.20.5.a1191-c
Subject(s) - offspring , fetus , medicine , endocrinology , fetal programming , intrauterine growth restriction , testosterone (patch) , gestation , pregnancy , biology , genetics
Fetal programming hypothesizes that insults during fetal life result in fetal adaptations leading to adult disease. Thus, the fetal environment is considered a factor in the etiology of hypertension (HT). Our laboratory has developed a unique model of intrauterine growth restriction (IUGR) induced by reduced uterine perfusion initiated by placement of silver clips around the abdominal aorta and ovarian arteries in late gestation. This model of fetal programming of hypertension demonstrates sex differences, as only adult male IUGR offspring are hypertensive. However, the purpose of this study was to determine if testosterone (T) contributes to the hypertension in male IUGR offspring. Mean arterial pressure (MAP) and T were significantly increased in male IUGR offspring as compared to male control offspring at 12 weeks of age (MAP measured in conscious, chronically instrumented animals: 139±2 vs. 129±2 mmHg and T: 399±75 vs. 166±30ng/ml, P<0.01, IUGR vs. control, respectively). Gonadectomy (CTX) performed at 10 weeks of age abolished hypertension in IUGR offspring (MAP measured by telemetry from 13 weeks: 137±1 vs. 117±1 to 16 weeks: 144±1 vs. 123±2 mmHg, CTX vs. Sham, respectively). Thus, these results suggest that testosterone does play a role in modulating hypertension in male IUGR offspring, thus providing an excellent animal model to study sex hormone involvement in the fetal programming of HT. NIH HL074927.