Local mechanisms within the intestine allow it to control its own blood flow independently of nervous or humoral influences. The evidence favoring the metabolic theory of local control is discussed within the framework of a two-component model in which a metabolic feedback signal from parenchymal cells maintains tissue oxygenation by two means: 1) by acting on arterioles to determine blood flow and capillary PO2 and 2) by opening or closing precapillary sphincters to regulate O2 extraction through changes in capillary surface area and diffusion distance. This purely metabolic model correctly predicts the observed responses of both resistance vessels and exchange vessels in most of the phenomena indicative of local control: functional hyperemia, reactive hyperemia, hypoxic vasodilation, pressure-flow autoregulation, and the enhanced pressure-flow autoregulation produced by lowering the prevailing O2 availability-to-demand ratio. The possibilities are discussed that interstitial hypoxia or adenosine might be the feedback signal in the metabolic regulation of intestinal blood flow.