Smoking is associated with multiple adverse pregnancy outcomes, including
fetal growth restriction. The objective of this study was to determine whether cigarette
smoke exposure during pregnancy in a mouse model affects the functional properties of maternal uterine, mesenteric, and renal arteries as a possible mechanism for growth restriction. C57Bl/CJ mice were exposed to whole body sidestream
smoke for 4 h/day.
Smoke particle exposure was increased from day 4 of gestation until late pregnancy (day 16-19), with mean total suspended particle levels of 63 mg/m(3), representative of moderate-to-heavy smoking in humans. Uterine, mesenteric, and renal arteries from late-pregnant and virgin mice were isolated and studied in a pressure-arteriograph system (n = 23). Plasma
cotinine was measured by ELISA.
Fetal weights were significantly reduced in
smoke-exposed compared with control fetuses (0.88 +/- 0.1 vs. 1.0 +/- 0.08 g, P < 0.02), while litter sizes were not different. Endothelium-mediated relaxation responses to
methacholine were significantly impaired in both the uterine and mesenteric vasculature of pregnant mice exposed to cigarette
smoke during gestation. This difference was not apparent in isolated renal arteries from pregnant mice exposed to cigarette
smoke; however, relaxation was significantly reduced in renal arteries from
smoke-exposed virgin mice. In conclusion, we found that passive cigarette
smoke exposure is associated with impaired vascular relaxation of uterine and mesenteric arteries in pregnant mice. Functional maternal vascular perturbations during pregnancy, specifically impaired peripheral and uterine vasodilation, may contribute to a mechanism by which smoking results in
fetal growth restriction.