OBJECTIVE to determine if morphological differences exist between vasculature shown to decompensate, ie, skeletal muscle (SM) and vasculature that maintains the compensatory effort, ie, cutaneous (C). METHODS dogs were anesthetized and subjected to a Wiggers hemorrhagic shock protocol. SM and C flows were monitored using electromagnetic flowmeters. Gracilis (SM) and saphenous (C) arterial segments were removed during: prehemorrhage control, compensation, and decompensation. Segments were fixed at in vivo intraluminal pressures. Both light and EM sections were made from each sample. RESULTS During the compensatory phase, both SM and C showed signs of strong vasoconstriction. Even though the amount of endothelial folding was comparable, the C did and the SM did not sustain the vasoconstriction. Vascular diameters of the SM but not C increased during decompensation. Ultrastructural changes consisted of extreme folding of the internal elastic lamina (IEL) during compensation and subsequent flattening out of the IEL during decompensation in the SM but not the C tissues. Cell deformation, damage, and exfoliation were seen in both SM and C tissues. CONCLUSIONS The data are consistent with the theory that SM vasculature, specifically endothelium, synthesizes an inhibitor of NE release, probably prostaglandins.