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Maternal protein restriction during pregnancy alters vasodilator mechanisms in fetal placental arteries (910.9)
Author(s) -
Sane Mukta,
Lekatz Leslie,
Shukla Praveen,
Vonnahme Kimberly,
O'Rourke Stephen
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.910.9
Subject(s) - medicine , endocrinology , vasodilation , enos , bradykinin , sodium nitroprusside , placenta , phenylephrine , fetus , receptor , pregnancy , chemistry , nitric oxide , biology , blood pressure , nitric oxide synthase , genetics
Maternal undernutrition during pregnancy reduces uterine blood flow. We hypothesized that reduced maternal protein intake during pregnancy alters vasodilator responses in placental arteries. Pregnant ewes were fed an isocaloric diet containing 100% (control) or 60% (protein‐restricted) of protein requirements from day 100‐130 of gestation (term= 145 d). Fetal placental arteries (FPA) were isolated on day 130. Sensitivity to bradykinin (BK)‐induced relaxation was increased 5‐fold in FPA from protein‐restricted ewes. In control FPA, BK‐induced relaxation was unaffected by indomethacin (Indo) but was inhibited by nitro‐l‐arginine (NLA). In FPA from protein‐restricted ewes, neither Indo nor NLA affected the response to BK. Sodium nitroprusside‐induced relaxation, phenylephrine (PE)‐induced contraction, and expression of eNOS, guanylyl cyclase (GC), and BK‐receptors, was similar in FPA from both dietary groups. In ewes fed a control diet, BK‐induced relaxation of FPA is mediated primarily by NO. In ewes fed a protein‐restricted diet, FPA are more sensitive than controls to BK‐induced relaxation and the mechanism is independent of NO and PGI2. The altered BK response is not due to changes in sensitivity to NO or PE, or to altered expression of eNOS, GC or BK receptors and may represent an adaptive mechanism to ensure adequate blood supply to the fetus during adverse maternal dietary conditions. Grant Funding Source : Supported by NIH