Nilton Hideto Takiuti

Stress-related preeclampsia: an evolutionary maladaptation in exaggerated stress during pregnancy?

The authors hypothesize that preeclampsia is a stress-related disease and an evolutionary maladaptation of exaggerated stress during human pregnancy. Epidemiologic studies show that relative risk for preeclampsia is increased in many stressful situations. Many risk factors for preeclampsia are stress-related. Low-stress situations, on the contrary, are protective. Stress in pregnancy corroborates all physiopathologic theories for preeclampsia; it does not contradict them. Animals exposed to intense stress show many characteristics of preeclampsia, and some animal models for human preeclampsia have been proposed. The stress-alarm reaction is protective for survival in animals. But the evolutionary maladaptation of this intense stress could lead to preeclampsia in humans.

The effect of chronic nitric oxide inhibition on vascular reactivity and blood pressure in pregnant rats

CONTEXT The exact mechanism involved in changes in blood pressure and peripheral vascular resistance during pregnancy is unknown. OBJECTIVE To evaluate the importance of endothelium-derived relaxing factor (EDRF) and its main component, nitric oxide, in blood pressure and vascular reactivity in pregnant rats. DESIGN Clinical trial in experimentation animals. SETTING University laboratory of Pharmacology. SAMPLE Female Wistar rats with normal blood pressure, weight (152 to 227 grams) and age (90 to 116 days). INTERVENTION The rats were divided in to four groups: pregnant rats treated with L-NAME (13 rats); pregnant control rats (8 rats); virgin rats treated with L-NAME (10 rats); virgin control rats (12 rats). The vascular preparations and caudal blood pressure were obtained at the end of pregnancy, or after the administration of L-NAME in virgin rats. MAIN MEASUREMENTS The caudal blood pressure and the vascular response to acetylcholine in pre-contracted aortic rings, both with and without endothelium, and the effect of nitric oxide inhibition, Nw-L-nitro-arginine methyl-ester (L-NAME), in pregnant and virgin rats. The L-NAME was administered in the drinking water over a 10-day period. RESULTS The blood pressure decreased in pregnancy. Aortic rings of pregnant rats were more sensitive to acetylcholine than those of virgin rats. After L-NAME treatment, the blood pressure increased and relaxation was blocked in both groups. The fetal-placental unit weight of the L-NAME group was lower than that of the control group. CONCLUSION Acetylcholine-induced vasorelaxation sensitivity was greater in pregnant rats and that blood pressure increased after L-NAME administration while the acetylcholine-induced vasorelaxation response was blocked.

Estresse e pré-eclampsia

A correlacao entre estresse e pre-eclampsia foi revisada, avaliada e discutida neste artigo.A pre-eclampsia nao tem ainda etiologia completamente definida. Varios fatores de risco para pre-eclampsia foram identificados e varios mecanismos fisiopatologicos foram descritos...

Expression of angiogenic factors in placenta of stressed rats

The aim of the present study was to analyse the influence of stress on pregnant rats, particularly in terms of maternal, placental and fetal weight, placental morphology and placental gene expression of the angiogenic factors Vegfa and Pgf and their receptors. The parameters were evaluated on gestation Day 20. Maternal, fetal and placental weights were statistically lower in stressed animals than controls, suggesting abnormalities in gestational physiology. Morphologically the placentas of rats subjected to stress were reduced in size and weight, with few glycogen cells and a significant increase in the number of apoptotic cells. Stress caused an increase in placental gene expression of Vegfa (P<0.05) and a reduction in Pgf, Flt1 and Kdr expression (P<0.05). It has been suggested that increased VEGF is associated with vasodilatation and hypotension, but in this model persistent hypertension was present. This study suggests that the limited hypotensive Vegfa response to stress-induced hypertension could result from reduced expression of Flt1/Kdr disrupting specific VEGF pathways. These findings may elucidate one of the multiple possible factors underlying how stress modulates placental physiology, and could aid the understanding of stress-induced gestational disorders.