Pravastatin Mitigates Hypertension, Proteinuria, and Fetal Growth Restriction in an L-NG-Nitro Arginine Methyl Ester (L-NAME)-Induced Rat Model of Preeclampsia.

BACKGROUND

Preeclampsia is a common pregnancy complication characterized by the abrupt onset of hypertension and proteinuria occurring after the midpoint of gestation. If left untreated, it can severely threaten the health of both the mother and the infant. This study aimed to evaluate the potential therapeutic effects of pravastatin in a rat model of preeclampsia. The study examined the efficacy of its ability to modulate key clinical and biochemical parameters, including blood pressure, proteinuria, nitric oxide concentrations, and the weights of the fetus and placenta.

METHODS

A total of 21 pregnant Wistar rats were divided into three groups: (1) a normal pregnant group; (2) a preeclamptic group (induced by a subcutaneous injection of L-NG-Nitro arginine methyl ester (L-NAME)); and (3) a preeclamptic group treated with pravastatin. The effects of pravastatin were evaluated on blood pressure and proteinuria, as well as its impact on endothelial function (serum nitric oxide) and birth outcomes (fetal and placental weights).

RESULTS

The results showed that L-NAME successfully created a preeclampsia model, which was marked by a notable rise in blood pressure and protein levels in urine, as well as a decrease in the weights of the fetus and placenta. The L-NAME group had reduced serum levels of nitric oxide, but the difference was not statistically significant. Conversely, pravastatin therapy entirely mitigated the detrimental effects of L-NAME. It resulted in significant reductions in blood pressure and proteinuria, along with increases in fetal and placental weights, plus an insignificant increase in nitric oxide levels.

CONCLUSION

Pravastatin demonstrates significant promise as a therapeutic intervention that can mitigate pathophysiological changes of an L-NAME-induced preeclampsia, such as hypertension, proteinuria, and diminished fetal and placental weights. Although the increase in serum nitric oxide levels did not reach statistical significance, the observed upward trend may reflect a partial restoration of endothelial function, which is typically impaired in this model. This suggests that pravastatin may exert a protective effect on the endothelium, at least in part, through modulation of NO pathways. Additional research, including clinical trials, is necessary to ascertain safety, optimal dosage, and long-term effects.