Investigators report that local heat causes an increase in skin blood flow consisting of two phases. The first is solely sensory neural, and the second is nitric oxide (NO)-mediated. We hypothesize that mechanisms behind these two phases are causally linked by shear stress. Because microvascular blood flow, endothelial shear stress and vessel diameters cannot be measured in humans, bat wing arterioles (26.6±0.3 µm, 42.0±0.4 µm, and 58.7±2.2 µm) were visualized non-invasively on a transparent heat plate via intravital microscopy. Increasing plate temperature from 25° C to 37° C increased flow in all three arterial sizes (137.1±0.3%, 251.9±0.5%, and 184.3±0.6%) in a biphasic manner. With heat, diameter increased in large arterioles (n=6) 8.7+0.03% within 6 min, medium arterioles (n=8) 19.7±0.5% within 4 min, and small arterioles (n=8) 31.6±2.2%, in the first min. Lidocaine (0.2 ml, 2% w/v) and L-NAME (0.2 ml, 1% w/v) was applied topically to arterioles (~40µm) to block sensory nerves, modulate shear stress and block NO generation. Local heat caused only a 10.4±5.5% increase in diameter with neural blockade (n=8) and only a 7.5±4.1% increase in diameter when flow was reduced (n=8), both significantly lower than control (p<0.001). Diameter and flow increases were significantly reduced with L-NAME application (p<0.05). Our novel thermoregulatory animal model illustrates 1) regulation of shear stress, 2) a non-neural component of the first phase, and 3) a shear-mediated second phase. The time course of dilation suggests early dilation of small arterioles increases flow and enhances second-phase dilation of the large arterioles.