Abstract 209: Hemeoxygenase-1 Induction Restores Beta ENaC Expression in Ischemic Placentas
Preeclampsia is a pregnancy-specific disease characterized by hypertension, proteinuria, and vascular abnormalities; the etiology of which is under active investigation. Utilizing the rat model of reduced uterine perfusion pressure (RUPP), our lab previously demonstrated that induction of hemeoxygenase-1 (HO-1) reduces blood pressure and oxidative stress in placental ischemic rats. While epithelial sodium channel proteins (specifically β-ENaC) are important in maintaining vascular myogenic tone and have been implicated in cytotropholast invasion, the effect of placental ischemia and induction of HO-1 on β-ENaC expression in placentas have not been established. Therefore, the purpose of this study is to test the hypothesis that placental β-ENaC expression is reduced in ischemic placentas and restored by HO-1 induction. Normal pregnant and RUPP rats were treated with the HO-1 inducer, cobalt protoporphyrin (CoPP) (n=4 per group/treatment). Blood pressure was measured and placentas were harvested on day 19 of gestation. Blood pressure increased from 101±1 to 141±4 mmHg (p<0.0001) in response to the RUPP procedure but was reduced by HO-1 induction (117±2 mmHg). RUPP rats also had fewer pups compared to normal pregnant rats (14±1 vs. 4±2 pups). HO-1 induction did not prevent the reduction in pup number. Placental β-ENaC protein expression was reduced by 62% in the RUPPs compared to the normal pregnant rats (p=0.036). HO-1 induction restored placental expression of β-ENaC to the levels of the normal pregnant rats. These findings suggest that HO-1 may exert its protective effects by altering the placental environment through changes in β-ENaC expression.
- © 2012 by American Heart Association, Inc.