Nitric oxide in the genesis of preeclampsia

The purpose of the investigation was to study nitric oxide (NO) in the genesis of preeclampsia (PE). Seventy-five pregnant women with preeclampsia, 23 with hypertensive disease, and 20 healthy pregnant women were examined. 24-hour blood pressure (BP) monitoring and an endothelium-dependent vasodilatation (EDVD) test were made; the levels of NO and dinitrazole complexes were determined. Inadequate NO release was ascertained to be one of the known causes of endothelial dysfunction. The ability of plasma to transfer NO becomes lower in preeclampsia, but it does not depend on its severity. NO release in the organs of pregnant animals with and without preeclampsia shows a circadian rhythm linked to diurnal BP variations and the decrease in the tissue content of NO in preeclamptic animals, as compared with healthy pregnant animals, points to the presence of vascular endothelial dysfunction. The correction of endothelial dysfunction is present in the spectrum of the pharmacological effects of nebivalol restoring an increment in the diameter of the brachial artery from 8.6 to 14.3% and the Ca antagonists nifedipine and amlodinine which increase the increment of EDVD to 12.4%.

preeclampsia, nitric oxide, endothelial dysfunction, vasodilatation