Serum from preeclamptic patients increases rat aorta vascular reactivity independent of endothelial nitric oxide and prostaglandins

Objective: To assess whether serum from preeclamptic patients increases vascular reactivity in an endothelium-dependent manner. Methods: Isolated rat thoracic aortae were incubated for 3 and 8 h in serum from preeclamptic patients, normotensive patients, or physiologic buffer. Vascular reactivity was assessed by phenylephrine-induced vasoconstriction in the presence and absence of N(ω)-nitro-L-arginine and indomethacin and by acetylcholine and S-nitroso-N-acetylpenicillamine-induced relaxation. Results: Aortae incubated in sera from preeclamptic patients showed a significant (P < 0.05) increase in sensitivity to phenylephrine (EC₅₀ = 7.71 ± 0.09, -log M) when compared with aortae incubated in normotensive sera (EC₅₀ 7.49 ± 0.08, -log M) or buffer (EC₅₀ = 7.41 + 0.08, -log M). After blocking nitric oxide production with N(ω)-nitro-L-arginine or after blocking prostaglandin production with indomethacin, vessels incubated in sera from preeclamptic patients remained more sensitive to phenylephrine than vessels incubated in sera from control patients. Acetylcholine-induced relaxation and S-nitroso-N-acetylpenicillamine concentration responses curves were not different. Conclusions: Serum from preeclamptic patients increases the sensitivity to phenylephrine. The increased sensitivity appears independent from endothelial nitric oxide or prostaglandin release. The serum-induced enhanced vascular smooth muscle reactivity therefore may be due to altered vascular smooth muscle function and not to altered endothelial function.