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Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Hypertension 2016 ; 67 (3): 647-53 Nephropedia Template TP
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Sildenafil treatment ameliorates the maternal syndrome of preeclampsia and rescues fetal growth in the Dahl Salt Sensitive rat #MMPMID26729752
Gillis EE; Mooney JN; Garrett MR; Granger JP; Sasser JM
Hypertension 2016[Mar]; 67 (3): 647-53 PMID26729752show ga
Preeclampsia, a hypertensive disorder of pregnancy, is detrimental to both mother and fetus. There is currently no effective treatment, but sildenafil, a phosphodiesterase-5 inhibitor, has been proposed as a potential therapy to reduce blood pressure and improve utero-placental perfusion in preeclamptic patients. We hypothesized that sildenafil would improve the maternal syndrome and fetal outcomes in the Dahl S rat model of superimposed preeclampsia. Dahl S rats were mated, and half received sildenafil (50 mg/kg/day, via food) from day 10 through day 20 of pregnancy. The untreated Dahl S rats had a significant rise in blood pressure and a 2-fold increase in urinary protein excretion from baseline to late pregnancy; however, sildenafil-treated Dahl S rats exhibited ~40 mmHg drops in blood pressure with no rise in protein excretion. Sildenafil also increased creatinine clearance and reduced nephrinuria and glomerulomegaly. Sildenafil treatment reduced the uterine artery resistance index during late pregnancy in the Dahl S rat and improved fetal outcomes (survival, weight, and litter size). Additionally, 19% of all pups were resorbed in untreated rats, with no incidence of resorptions observed in the treated group. Furthermore, TNF-?, endothelin-1, and oxidative stress, which are characteristically increased in women with preeclampsia and in experimental models of the disease, were reduced in treated rats. These data suggest that sildenafil improves the maternal syndrome of preeclampsia and blood flow to the fetoplacental unit, providing preclinical evidence to support the hypothesis that PDE-5 inhibition may be an important therapeutic target for the treatment of preeclampsia.