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Abnormal endothelial cell function of resistance arteries from women with preeclampsia
A L McCarthy1, R G Woolfson, S K Raju
1UMDS Smooth Muscle Group, Sherrington School of Physiology, Guy's Hospital, London, England.
Objective:
There is substantial indirect evidence that the vascular endothelium may be dysfunctional in preeclampsia and that reduced production of endothelial-derived vasodilators may account for the increased vascular resistance and enhanced pressor sensitivity characteristic of this disorder. In this study we directly investigated endothelial function by examining acetylcholine-mediated relaxation in small arteries dissected from the subcutaneous fat layer examined at the time of cesarean section.
Study Design:
By means of a small vessel myograph we measured tension in resistance arteries of normal pregnant women (n = 12) and women with preeclampsia (n = 12) and assessed the contributions of vasodilatory prostanoids and endothelium-derived relaxing factor to endothelium-dependent relaxation, as elicited by acetylcholine, 1 nmol/L to 10 mumol/L, after precontraction with 3 mumol/L norepinephrine.
Results:
Endothelium-dependent relaxation was impaired in arteries of women with preeclampsia compared with arteries from normotensive pregnant women. Endothelium-independent relaxation as assessed by sodium nitroprusside was not altered in the arteries from preeclamptic women.
Conclusions:
This study provides direct evidence of abnormal endothelial function in preeclampsia. No deficiency in endothelium-independent relaxation could be detected.