Menopause (New York, N.Y.) · 2026
Postmenopausal vasomotor symptoms are associated with heightened cutaneous vasodilation despite preserved nitric oxide-mediated endothelial function.
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Li-Maloney Caroline, McGarr Gregory W, Fujii Naoto, Amano Tatsuro, Kenny Glen P
Аннотация
OBJECTIVE: To evaluate whether postmenopausal females with vasomotor symptoms (VMS) exhibit altered nitric oxide synthase (NOS)-dependent cutaneous vasodilation during local heating, and whether these responses vary by body region.
METHODS: Cutaneous vascular conductance normalized to maximum vasodilation (percentage of the maximal conductance [%CVCmax]) was assessed at the chest, abdomen, forearm, and calf using laser-Doppler flowmetry in 18 postmenopausal females (9 with current VMS, 9 without VMS). Local skin temperature was increased from 33 °C to 42 °C (~30 min) to elicit a vasodilatory plateau. NG-nitro-L-arginine methyl ester (20 mM), a NOS inhibitor, was then perfused during continued heating (~40 min). The NOS contribution was assessed by the difference in %CVCmax mediated by NG-nitro-L-arginine methyl ester.
RESULTS: Baseline %CVCmax was higher at the chest compared with the calf across groups (10.0 [3.3, 16.6]%; P = 0.0013). During the 42 °C heating plateau, females with VMS exhibited greater %CVCmax than those without VMS when responses were pooled across regions (7.2 [1.7, 23.5]%; P = 0.013), and at the abdomen (8.7 [0.6, 18.4]%), chest (10.3 [2.3, 18.4]%), and calf (8.4 [0.4, 16.5]%; all P < 0.036). However, the NOS-mediated contribution did not differ between groups or across regions (all P > 0.15).
CONCLUSION: Although postmenopausal females with VMS exhibit heightened cutaneous vasodilatory responses to local heating, NOS-dependent vasodilation is preserved. These findings suggest that enhanced microvascular reactivity in VMS is not attributable to altered endothelial NOS function.
METHODS: Cutaneous vascular conductance normalized to maximum vasodilation (percentage of the maximal conductance [%CVCmax]) was assessed at the chest, abdomen, forearm, and calf using laser-Doppler flowmetry in 18 postmenopausal females (9 with current VMS, 9 without VMS). Local skin temperature was increased from 33 °C to 42 °C (~30 min) to elicit a vasodilatory plateau. NG-nitro-L-arginine methyl ester (20 mM), a NOS inhibitor, was then perfused during continued heating (~40 min). The NOS contribution was assessed by the difference in %CVCmax mediated by NG-nitro-L-arginine methyl ester.
RESULTS: Baseline %CVCmax was higher at the chest compared with the calf across groups (10.0 [3.3, 16.6]%; P = 0.0013). During the 42 °C heating plateau, females with VMS exhibited greater %CVCmax than those without VMS when responses were pooled across regions (7.2 [1.7, 23.5]%; P = 0.013), and at the abdomen (8.7 [0.6, 18.4]%), chest (10.3 [2.3, 18.4]%), and calf (8.4 [0.4, 16.5]%; all P < 0.036). However, the NOS-mediated contribution did not differ between groups or across regions (all P > 0.15).
CONCLUSION: Although postmenopausal females with VMS exhibit heightened cutaneous vasodilatory responses to local heating, NOS-dependent vasodilation is preserved. These findings suggest that enhanced microvascular reactivity in VMS is not attributable to altered endothelial NOS function.