Therefore, we analyzed the reactivity of third order arteries (similar to 200 mu m) from the CA membrane of 15 and 19 day chicken embryos. CA arteries contracted in response to K(+), the thromboxane A(2) mimetic U46619, endothelin-1, acetylcholine and acute hypoxia, but showed no reaction to alpha-adrenergic stimulation (phenylephrine). The nitric oxide donor sodium nitroprusside, the adenylyl cyclase agonist forskolin, and the beta-adrenergic agonist isoproterenol relaxed CA arteries precontracted with K(+) or U46619. The contraction evoked by acetylcholine and the relaxations

selleckchem evoked by sodium nitroprusside and isoproterenol decreased with incubation age. In conclusion, CA arteries share many characteristics with human fetoplacental arteries, such as pronounced relaxation to beta-adrenergic stimuli and hypoxic vasoconstriction. Our study will be

the foundation for future studies to explain disparate and common responses of the CA and fetoplacental vasculature.”
“Preeclampsia is a major obstetric problem AZD4547 defined by new-onset hypertension and proteinuria associated with compromised placental perfusion. Although activation of the complement system is increased in preeclampsia compared to normal pregnancy, it remains unclear whether excess complement activation is a cause or consequence of placental ischemia. Therefore, we hypothesized that complement activation is critical for placental ischemia-induced hypertension. We employed the reduced utero-placental perfusion pressure (RUPP) model of

placental ischemia in the rat to induce hypertension in the third trimester and evaluated the effect of inhibiting complement activation with a soluble recombinant form of an endogenous complement regulator, human complement receptor 1 (sCR1; CDX-1135). On day 14 of a 21-day gestation, rats SB202190 inhibitor received either RUPP or Sham surgery and 15 mg/kg/day sCR1 or saline intravenously on days 14-18. Circulating complement component 3 decreased and complement activation product C3a increased in RUPP vs. Sham (p < 0.05), indicating complement activation had occurred. Mean arterial pressure (MAP) measured on day 19 increased in RUPP vs. Sham rats (109.8 +/- 2.8 mmHg vs. 93.6 +/- 1.6 mmHg). Treatment with sCR1 significantly reduced elevated MAP in RUPP rats (98.4 +/- 3.6 mmHg, p < 0.05) and reduced C3a production. Vascular endothelial growth factor (VEGF) decreased in RUPP compared to Sham rats, and the decrease in VEGF was not affected by sCR1 treatment. Thus, these studies have identified a mechanistic link between complement activation and the pregnancy complication of hypertension apart from free plasma VEGF and have identified complement inhibition as a potential treatment strategy for placental ischemia-induced hypertension in preeclampsia. (C) 2013 Elsevier Ltd. All rights reserved.