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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