Fig. 2
From: Neurovascular dysfunction in vascular dementia, Alzheimer’s and atherosclerosis
Neurophysiology of neurovascular coupling overview. Neural activity is metabolically expensive demanding a high consumption of glucose and oxygen (from arterial blood). Simultaneously, CO2 and other by products are also produced, which need to be removed by diffusion into venous blood in order to prevent hypercapnia and acidosis. In order to achieve this, neurons regulate blood flow via neurovascular coupling. Vasoactive agents such as NO directly cause vasodilation of arterial smooth muscle cells. Significant neurogliovascular signalling involving glutamate and calcium signalling causes vasodilation via channels on VSMCs e.g. BKCa, TRPV4, to stimulate cGMP [105]. There are indeed multiple and complex signalling pathways (including ATP and VIP signalling) also involved in neurovascular coupling. In addition to vasodilator signals, vasoconstrictive signals are also produced, namely 20-HETE, however this is thought to be pathological and as a result of ageing [106]. Pericytes regulate capillary diameter by responding to glutamate release, in addition to PGE2 produced by astrocytes