Women with a history of preeclampsia have preserved sensory nerve‐mediated dilation in the cutaneous microvasculature

Abstract

Women who have had preeclampsia (PE) 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 sensory nerve-mediated initial peak, followed by a sustained endothelium-dependent plateau. We have previously shown that the endothelium-dependent plateau is attenuated in PE. However, it is unknown if the sensory nerve-mediated initial peak is similarly attenuated. Therefore, the purpose of this study was to examine the effect of preeclampsia history on sensory nerve-mediated vasodilation and the NO-dependent contribution to that response. We hypothesized that PE would have an attenuated initial peak and a reduced NO-dependent contribution to that response compared to women with a history of normotensive pregnancy (HC). Nine HC (31 ± 4yrs) and 9 PE (28 ± 6yrs) 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). There were no differences in the initial peak between groups (HC: 79 ± 8 vs PE: 80 ± 10%CVCmax; p = 0.936). NOS-inhibition attenuated the initial peak in both HC (57 ± 18%CVCmax; p = 0.003) and PE (54 ± 10%CVCmax; p = 0.002). However, there were no differences in the NO-dependent portion of initial peak (HC: 23 ± 16 vs PE: 24 ± 9%; p = 0.777). The local heating plateau (HC: 99 ± 4 vs PE: 88 ± 7%CVCmax; p = 0.001) and NO-contribution to the plateau (HC: 31 ± 9 vs PE: 17 ± 14%; p = 0.02) were attenuated in PE. There was no relation between NO-dependent dilation in the initial peak and NO-dependent dilation in the plateau across groups (R2 = 0.005; P = 0.943). Women who have had preeclampsia demonstrate attenuated microvascular endothelium-dependent dilation. However, there are no differences in sensory nerve-mediated vasodilation following preeclampsia, suggesting that the NO-dependent vasodilation of the neurogenic response is not related to endothelium-dependent NO-mediated dilation in these women.

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