Women with a history of preeclampsia (hxPE) demonstrate persistent microvascular endothelial dysfunction which may contribute to the progression of cardiovascular disease. Women with hxPE also have higher rates of depression compared to women with a history of healthy pregnancy. Interestingly, accumulating evidence indicates that antidepressant treatment may have vasculoprotective effects and attenuate preeclampsia risk. However, whether antidepressant treatment impacts microvascular function in these women remains unknown. Therefore, we examined the effect of chronic antidepressant use on microvascular function in women with hxPE. We hypothesized that antidepressant-treated women with hxPE would have greater endothelium-mediated microvascular vasodilation than unmedicated women with hxPE. Five women with hxPE who were currently treated with an antidepressant (hxPE+AD; 36±3 years; 26±7 months postpartum), six who were not (hxPE-AD; 34±2 years; 26±5 months postpartum), and six unmedicated women with a history of uncomplicated pregnancy (HC; 37±1 years; 35±7 months postpartum) participated in one study visit. We measured cutaneous vascular conductance (CVC=laser doppler flowmetry flux/MAP) responses to graded perfusion of acetylcholine (10−10-10−1 mM) via microdialysis in a control (lactated Ringer's) site and a site treated with 15 mM NG-nitro-L-arginine methyl ester [L-NAME; nitric oxide (NO) synthase inhibitor]. hxPE-AD had reduced endothelium-dependent dilation compared to HC (acetylcholine ³10−3 mM; P<0.03). hxPE+AD had greater endothelium-dependent dilation compared to hxPE-AD (acetylcholine 10−2 and 10−3 mM; P<0.02) and there were no differences between hxPE+AD and HC (all P>0.05). L-NAME reduced endothelium-dependent dilation in all groups (all P<0.001), and there was no difference between groups in NO-dependent dilation [area under the curve (AUC) at a control site − AUC at a L-NAME treated site; P=0.522]. These data suggest that microvascular endothelium-dependent dilation is preserved in women with a history of preeclampsia treated with an antidepressant, potentially mediated through non-NO-dependent mechanisms. Funding: American Heart Association CDA 937990. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
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