Women with a History of Preeclampsia Have Preserved Neurogenically‐Mediated Dilation in the Cutaneous Microvasculature

Michael Pyevich; Lacy Alexander; Anna Stanhewicz

doi:10.1096/fasebj.2021.35.S1.02316

Women who have had preeclampsia (PrEC) demonstrate microvascular endothelial dysfunction, mediated in part by reduced nitric oxide (NO)‐dependent mechanisms. Localized heating of the skin induces a biphasic vasodilation response: a neurogenically‐mediated initial peak, followed by a sustained endothelium‐dependent plateau. We have previously shown that the endothelium‐dependent plateau is attenuated in PrEC, due to attenuated NO‐dependent dilation. However, it is unknown if the same is true concerning the neurogenically‐mediated initial peak. The purpose of this study was to (1) examine the effect of preeclampsia history on neurogenically‐mediated vasodilation and the NO‐dependent contribution to that response, and (2) examine the relation between NO‐dependent neurogenic dilation and the NO‐dependent portion of the endothelium‐dependent plateau. We hypothesized that PrEC would have an attenuated initial peak response and a reduced NO‐dependent contribution to that response compared to women with a history of normotensive pregnancy (HC). Six HC (31±2yrs, 7±2 months post‐partum) and 7 PrEC (29±2yrs, 7±3months post‐partum) underwent a standard local heating protocol (42°C; 0.1°C·s‐1). Two intradermal microdialysis fibers were placed in the skin of the ventral forearm for the continuous local delivery of Lactated Ringer's alone (control) or 15mM NG‐nitro‐L‐arginine methyl ester (L‐NAME) for nitric oxide synthase (NOS)‐inhibition. Red blood cell flux was measured at each site via laser‐Doppler flowmetry (LDF). Cutaneous vascular conductance was calculated (CVC=LDF/mean arterial pressure) and normalized to maximum (%CVCmax; 28mM SNP + local heat 43°C). NO‐dependent dilation was calculated within‐subject as the difference between control and NOS‐inhibited sites. There were no differences in the initial peak between groups (HC: 80±5 vs PrEC: 79±5 %CVCmax; p=.88). NOS‐inhibition attenuated the initial peak in both HC (Control: 80±5 vs L‐NAME: 57±9 %CVCmax; p=0.02) and PrEC (Control: 79±5 vs L‐NAME: 53±6 %CVCmax; p=0.004). However, there were no group differences in the NO‐dependent portion of initial peak (HC: 23±8 vs PrEC: 24±5 %CVCmax; p=0.97). The local heating plateau (HC: 99±2 vs PrEC: 85±1 %CVCmax; p<0.001) and NO‐contribution to the plateau (HC: 47±5 vs PrEC: 14±5 %CVCmax; p<0.001) were attenuated in PrEC compared to HC. There was no relation between NO‐dependent dilation in the initial peak and NO‐dependent dilation in the plateau across groups (R2 = 0.05; p = 0.51). Women who have had preeclampsia demonstrate attenuated microvascular endothelium‐dependent dilation compared to women with a history of uncomplicated pregnancy. However, there are no differences in neurogenically‐mediated vasodilation between the groups, suggesting that the NO‐dependent vasodilation of the neurogenic response is not related to endothelium‐dependent NO‐mediated dilation in these women.

Women with a History of Preeclampsia Have Preserved Neurogenically‐Mediated Dilation in the Cutaneous Microvasculature

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