The cardiovascular response to feeding consists of two phases. The anticipation/ingestion phase is a brief, generalized cardiovascular response mediated by sympathetic neural activity. The digestive/absorptive phase is a longer, locally mediated vascular response to luminal nutrients. This post-prandial hyperaemia is localized primarily to the intestinal segment and tissue layer (mucosa) exposed to chyme. The stimuli for this hyperaemia are the digested products of food, and bile. Micellar fatty acids induce the greatest hyperaemia, followed by glucose. Individual amino acids have little effect, but by-products of protein digestion may increase blood flow. Bile enhances the glucose-induced hyperaemia and renders fatty acids and amino acids vasoactive. The mechanisms involved in the initiation and maintenance of the hyperaemia are complex and involve numerous factors that may vary with the type of nutrient. The factors involved include intestinal activity such as absorption, motility and secretion, tissue oxidative metabolism, adenosine, tissue oxygen tension, the enteric nervous system, gastrointestinal peptides such as vasoactive intestinal polypeptide, and paracrine substances such as histamine and prostanoids. The post prandial intestinal hyperaemia is probably the net result of the complex interaction of all these factors on the intestinal vascular smooth muscle.