Experimental preeclampsia in rats affects vascular gene expression patterns.

Normal pregnancy requires adaptations of the maternal vasculature. During preeclampsia these adaptations are not well established, which may be related to maternal hypertension and proteinuria. The effects of preeclampsia on the maternal vasculature are not yet fully understood.

Regional distribution of cerebral white matter lesions years after preeclampsia and eclampsia.

Objective: To assess the distribution of cerebral white matter lesions in women who had eclampsia, preeclampsia, or normotensive pregnancies. The pathophysiology of these lesions, more often seen in formerly eclamptic and preeclamptic women, is unclear but may be related to a predisposition for vascular disease, the occurrence of the posterior reversible encephalopathy syndrome, or both while pregnant. Assessing the distribution of such lesions may give insight into their pathophysiology and possible consequences.

Endothelium-dependent relaxation and angiotensin II sensitivity in experimental preeclampsia.

Objective: We investigated endothelial dysfunction and the role of angiotensin (Ang)-II type I (AT1-R) and type II (AT2-R) receptor in the changes in the Ang-II sensitivity in experimental preeclampsia in the rat.

Methods: Aortic rings were isolated from low dose lipopolysaccharide (LPS) infused pregnant rats (experimental preeclampsia; n=9), saline-infused pregnant rats (n=8), and saline (n=8) and LPS (n=8) infused non-pregnant rats. Endothelium-dependent acetylcholine-mediated relaxation was studied in phenylephrine-preconstricted aortic rings in the presence of vehicle, N(G)-nitro-L-arginine methyl ester and/or indomethacin.

Structure and function of cerebral and mesenteric resistance arteries in low-dose endotoxin-infused pregnant rats.

Objective: Since the cerebrovasculature likely plays a prominent role in the pathophysiology of eclampsia, we assessed the effects of low-dose endotoxin-induced experimental preeclampsia on the function and structure of rat posterior cerebral arteries (PCA) and mesenteric arteries (MA).

Methods: Nonpregnant (NP) and pregnant (P) rats were infused with saline (NP-CTL, n=9; P-CTL, n=9) or low-dose endotoxin (NP-endotoxin, n=9; P-endotoxin, n=10). Myogenic activity, pressure of forced dilatation (FD) and structural properties were evaluated in PCA and MA.