The hypothesis that the increase in post-prandial splanchnic blood flow will be reduced during hypoxia to prioritise blood flow to other organs was tested by measuring cardiac output and gut blood flow during a stepwise hypoxic challenge (five steps, from 20.6 to 3.9 kPa, 5 min of exposure to each level) before and after feeding (equivalent to 2.9% of body mass). Splanchnic blood flow, both absolute and relative to cardiac output, increased after feeding. Mean post-prandial gut blood flow increased by 71% (from 9.6+/-1.6 to 14.9+/-1.6 ml min(-1) kg(-1), means +/- S.E.M.). Before feeding, gut blood flow was 24.0% of cardiac output, and this increased significantly 24 h after feeding to 34.0%. The absolute post-prandial increase in gut blood flow (5.3+/-0.9 ml min(-1) kg(-1)) was paralleled by an increase in cardiac output (5.4+/-2.1 ml min(-1) kg(-1)). Hypoxia decreased gut blood flow significantly from 9.6+/-1.6 to 3.7+/-1.1 ml min(-1) kg(-1), corresponding to a decrease in relative gut blood flow from 24 % to 13%. Contrary to our initial hypothesis, and although post-prandial absolute blood flow decreases during hypoxia, the relative proportion of cardiac output reaching the gut did not decrease (34.6% pre-hypoxia versus 26.7% during hypoxia), unlike the situation in non-feeding fish. We propose that, following feeding, relative gut blood flow is maintained because splanchnic hyperaemia occurs as a result of the release of local factors; consequently the reflex vasoconstriction of the gastrointestinal vasculature during hypoxia is not as effective in decreasing gut blood flow as it was before feeding because local hyperaemia out-competes the reflex regulation.