Abstract 67

Aim: To study the effect of a pharmacological model of preeclampsia induced by nitric oxide synthase (NOS) inhibition with L-NAME, on the endothelium-dependent relaxation induced by acetylcholine (ACh) of fetuses and newborns. Materials: Wistar rats received L-NAME (0.5 mg/mL drinking water) from 10th to 21h day of pregnancy, or until the 2nd postpartum day, resulting in proteinuric hypertension; untreated rats remained as controls. At the end of these periods, fetuses (FET) - obtained by laparotomy- or 2-day-old breast-feeded newborns (NWB) were killed, their aorta isolated and mounted on wires in a myograph. Measurements: The relaxation to 1 µM ACh was expressed in % precontraction with 3 µM prostaglandin F2a (PGF2a) or 50 mM KCl. Results: ACh relaxation, expressed as mean ± SEM of 18-40 experiments [(*) p<0.05 vs FET, (†) vs control, and (#) vs PGF2a by t test] (Table) Conclusions: In rats, a preeclampsia-like model (chronic NOS inhibition) impairs ACh-induced relaxation of aortic segments from fetuses but not newborns, suggesting that some maternal factor could affect fetal arteries.

Table 1 No caption available.
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Supported by Grants from DGICYT (PM 97/0008), FISS (98/0074-02) and Bayer España.