SERUM FROM PREECLAMPTIC PATIENTS INCREASES RAT AORTA VASCULAR REACTIVITY INDEPENDENT OF ENDOTHELIAL NITRIC-OXIDE AND PROSTAGLANDINS

Objective: To assess whether serum from preeclamptic patients increase s vascular reactivity in an endothelium-dependent manner. Methods: iso lated rat thoracic aortae were incubated for 3 and 8 h in serum from p reeclamptic patients, normotensive patients, or physiologic buffer. Va scular reactivity was assessed by phenylephrine-induced vasoconstricti on in the presence and absence of N-omega-nitro-L-arginine and indomet hacin and by acetylcholine and S-nitroso-N-acetylpenicillamine-induced relaxation. Results: Aortae incubated in sera from preeclamptic patie nts showed a significant (P < 0.05) increase in sensitivity to phenyle phrine (EC50 = 7.71 +/- 0.09, -log M) when compared with aortae incuba ted in normotensive sera(EC,, = 7.49 +/- 0.08, -log M) or buffer (EC50 = 7.41 0.08, -log M). After blocking nitric oxide production with N-o mega-nitro-L-arginine or after blacking prostaglandin production with indomethacin, vessels incubated in sera from preeclamptic patients rem ained more sensitive to phenylephrine than vessels incubated in sera f rom control patients. Acetylcholine induced relaxation and S-nitroso-N -acetylpenicillamine concentration responses curves were not different . Conclusions: Serum from preeclamptic patients increases the sensitiv ity to phenylephrine. The increased sensitivity appears independent fr om endothelial nitric oxide or prostaglandin release. The serum-induce d enhanced vascular smooth muscle reactivity therefore may be due to a ltered vascular smooth muscle function and not to altered endothelial function.