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Mechanisms underlying the reduced endothelium-dependent relaxation in human omental resistance artery in pre-eclampsia

Yoshikatsu Suzuki*†, Junko Kajikuri†, Kaoru Suzumori* and Takeo Itoh†

1. In pre-eclampsia, a functional change occurs in the role played by endothelium-derived nitric oxide (NO) in the regulation of smooth muscle contraction in resistance arteries. We investigated the underlying mechanism in human omental resistance arteries from normotensive pregnant and pre-eclamptic women in the presence of diclofenac (an inhibitor of cyclo-oxygenase).

2. In endothelium-intact strips, the sensitivity to 9,11-epithio-11,12-methano-thromboxane A₂ (STA₂) was significantly higher in pre-eclampsia, and this was not modified by either N^G-nitro-L-arginine (L-NNA, an inhibitor of NO synthase) or removal of the endothelium.

3. Bradykinin and substance P each produced an endothelium-dependent relaxation of the STA₂-induced contraction in both groups, although the relaxation was significantly smaller for pre-eclampsia. L-NNA markedly attenuated the endothelium-dependent relaxation in the normotensive pregnant group but not in the pre-eclamptic group.

4. In the presence of L-NNA, the relaxation induced by sodium nitroprusside (SNP) on the STA₂ contraction was significantly smaller for pre-eclamptic than for normotensive pregnant women.

5. In endothelium-denuded strips, the relaxation induced by 8-para-chlorophenyl thio-guanosine-3',5'-cyclic monophosphate (8-pCPT-cGMP) on the STA₂ contraction was significantly less for pre-eclampsia.

6. In -escin-skinned strips from both groups of women, 8-pCPT-cGMP (1-10 µM) concentration-dependently attenuated the contraction induced by 0·5 µM Ca²⁺. However, its relaxing action was significantly weaker in pre-eclampsia.

7. It is suggested that the weaker responsiveness to NO seen in strips from pre-eclamptic women may be partly due to a reduced smooth muscle responsiveness to cyclic GMP.

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