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Neutrophil depletion attenuates placental ischemia‐induced hypertension in rat
Author(s) -
Lillegard Kathryn E,
Bauer Ashley J,
Johnson Alex C,
Lojovich Sarah J,
Gilbert Jeffrey S,
Regal Jean F
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.907.4
Subject(s) - endocrinology , medicine , preeclampsia , ischemia , perfusion , gestation , placenta , vascular endothelial growth factor , mean arterial pressure , blood pressure , fetus , pregnancy , biology , vegf receptors , heart rate , genetics
Preeclampsia is characterized by compromised placental perfusion and hypertension during pregnancy. Preeclamptic women exhibit a greater number of neutrophils (PMN) in the vasculature and a decrease in plasma free vascular endothelial growth factor (VEGF) compared to normal pregnancy. Hypothesis PMN are critical to placental ischemia‐induced hypertension and decreased VEGF. Using the reduced uterine perfusion pressure (RUPP) model of placental ischemia‐induced hypertension, we determined the effect of PMN depletion on blood pressure and plasma VEGF. PMN were depleted with repeated injections of polyclonal rabbit anti‐rat neutrophil antibody (αPMN). On gestation day 14, clips were placed on the abdominal aorta and uterine arteries to decrease placental perfusion. RUPP and Sham rats received either αPMN or normal rabbit serum (Ctl) on gestation days 13, 14, 16, and 18, and mean arterial pressure (MAP) was measured via arterial catheter on day 19. PMN‐depleted rats had reduced circulating PMN (p<0.05) on day 14 compared to Ctl. MAP increased (p<0.05) in RUPP Ctl vs Sham Ctl rats, and PMN depletion attenuated this increase in MAP in RUPP rats (p=0.04) without any effect on Sham rats. The RUPP‐induced decrease in VEGF was not affected by PMN depletion. Thus, neutrophils are important in placental ischemia‐induced hypertension independent of plasma free VEGF concentrations. Support: NIH R15 HL109843.

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