Functional hyperaemia is an increase in blood flow to a tissue due to the presence of metabolites and a change in general conditions.
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)).
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.
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.
[5] Conversely, when a tissue is less metabolically active, it produces fewer metabolites which are simply washed away in blood flow.
Subsequently, there is an increased blood flow to the affected area, aimed at eliminating waste products and clearing cellular debris.