Hyperaemia is likely mediated by the increased synthesis and/or release of vasodilatory agents during periods of heightened cellular metabolism. The increase in cellular metabolism causes the increase in vasoactive metabolic byproducts. Some of the putative vasodilatory agents (associated with metabolism) include, but are not limited to: carbon dioxide (CO2), hydrogen ion (H+), potassium (K+), adenosine (ADO), nitric oxide (NO)). These vasodilators released from the tissue act on local arterioles causing vasodilation, this causes a decrease in vascular resistance and allows an increase in blood flow to be directed toward the capillary bed of the active tissue. This increase allows the blood to serve the increased metabolic demand of the tissue and prevents a mismatch between O2-demand O2-supply. Recent research has suggested that the locally produced vasodilators may be acting in a redundant manner, in which the antagonism of one dilator, be it pharmacologically or pathologically, may be compensated for by another in order to preserve blood flow to tissue. While the locus of blood flow control (at least in skeletal muscle tissue) is widely thought to reside at the level of the arteriole, research has begun to suggest that capillary endothelial cells may be coordinators of skeletal muscle blood flow during functional hyperaemia. It is thought that vasodilators (released from active muscle fibers) can stimulate a local capillary endothelial cells which, in turn, causes the conduction of a vasodilatory signal to upstream arterioles, this then elicits arteriolar vasodilation consequently, creating a pathway of least resistance so blood flow can be precisely direct to capillaries supplying the metabolically active tissue.