Vaginal lubrication is reliant upon healthy blood flow because vaginal lubrication is ultrafiltrated blood.
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The vagina contains no glands.
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Blood pressure pushes fluid from the capillaries through intracellular gap junctions between vaginal epithelial cells. The resultant vaginal transudate is mainly composed of water and very small proteins, which combine at the vaginal surface with dead epithelial cells.
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Sufficient pelvic blood flow is dependent on the bioavailability of nitric oxide. Gaseous is produced in capillary endothelia in response to shear stress or vibration or in response to sexual arousal via parasympathetic nitrergic nerves. Once produced,  induces vasodilation through a cyclic guanosine monophosphate (cGMP) cascade, which diminishes as phosphodiesterase enzymes subdue the effect.
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Therefore, vaginal lubrication production depends upon the synthesis, enzymatic facilitation, and bioavailability. The enzymatic function of synthase is enhanced by steroid hormones, most notably estrogen in a rapid-action nongenomic effect. 
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Importantly, the presence of NO is not sufficient for its effect. Many biological feedback mechanisms exist to suppress the production of NO as high production of NO in an inflammatory environment can lead to irreversible free radical production. Metabolic conditions of low inflammation are supportive to the bioavailability of NO in facilitating vaginal lubrication.
The vagina’s lubrication does not come from glands but from a transudative fluid expressed through vaginal epithelial cells from filtered blood that requires adequate perfusion and NO