[The metabolic regulation of cerebral microcirculation]

To analyse the mechanisms involved in the microvascular metabolic regulation of cerebral blood flow. The article outlines the neuronal metabolism and mechanisms involved in functional hyperaemia and examines the contractile properties of brain microvasculature. It also discusses the role played by ion channels in pericytes and vascular smooth muscle and describes the signalling pathways involved in arteriolar and capillary vasodilatation or vasoconstriction.

The blood-brain barrier and the close functional relations between neurons and astrocytes give rise to nerve tissue properties such as functional hyperaemia. In this mechanism the astrocytes act as a structural and functional 'bridge' between neurons and brain capillaries, and respond to synaptic activity by releasing vasoactive compounds, above all vasodilators. The metabolites derived from arachidonic acid, such as prostaglandins and epoxyeicosatrienoic acids, as well as the compounds that have traditionally been involved, such as nitric oxide and prostacyclin, are especially important. These substances are capable of extending to the capillaries and arterioles, where they alter the membrane potential and the contractibility of the pericytes and the smooth muscle of vessels.

The functional interaction among neurons, astrocytes and capillaries in the central nervous system (called the 'neurovascular unit') is essential for the regulation of cerebral blood flow, since it links neuron-glial cell metabolic activity to the supply of energetic substrates from the microcirculation. Within this functional unit, astrocytes play a vital role by releasing vasoactive substances that are derived from or produced by neuronal activity.