The extrinsic innervation of cerebral (pial) vessels consists of components of the autonomic nervous system. Cervical sympathetic nerve fibers that accompany the internal carotid and vertebral arteries into the cranial cavity innervate the cerebral vessels. In comparison to other vascular beds, sympathetic control of the cerebral vessels is weak, and the contractile state of the cerebrovascular smooth muscle depends primarily on local metabolic factors. The density of α1-adrenergic receptors is less than in other vascular beds. Cerebral vessels receive parasympathetic fibers from the facial nerve that produce a slight vasodilation
Controls: rest Sens 1 Sens 2 •Fig. 17.41 Effects of Different Stimuli on Regional Blood Flow in the Contralateral Human Cerebral Cortex. Sens1,low-intensityelectricalstimulationofthehand;Sens2,high-intensity(painful)electricalstimulationofthehand.Otherstimuliareasnoted.(RedrawnfromIngvarDH.Brain Res. 1976;107:181.) on stimulation. The sympathetic nervous system exerts the most prominent effect on cerebral blood flow during pathophysiological conditions.
In general, total cerebral blood flow is relatively constant and is autoregulated. Autoregulation of cerebral blood flow involves interplay among myogenic, metabolic, and neural mechanisms much as described for peripheral vessels (see ). However, regional blood flow in the brain is associated with regional neural activity. For example, movement of one hand results in increased blood flow only in the hand area of the contralateral sensorimotor and premotor cortex. Talking, reading, and other stimuli to the cerebral cortex are also associated with increased blood flow in the appropriate regions of the contralateral cortex (
Fig.
17.41 ). Glucose uptake also corresponds to regional cortical neuronal activity. Thus when the retina is stimulated by light, uptake of glucose is enhanced in the visual cortex.
The neurovascular unit plays an integral role in the discrete regulation of blood flow. Production of vasoactive compounds couples increased neuronal activity to greater uptake of oxygen and glucose. Within the neurovascular unit, astrocytes link neurons with the microcirculation (see
Fig. 17.40 ). At one pole, astrocytes surround presynaptic and postsynaptic neurons at synapses. At the other pole, astrocytes converge on vascular smooth muscle and endothelial cells of cerebral vessels. When activated by the neurotransmitter glutamate or acetylcholine, astrocytes produce inositol trisphosphate (IP3), which causes the release of Ca++, which, in turn, activates large conductance potassium (BKCa) channels. The released K+ raises extracellular [K+] to 8 to 15 mEq/L in the space between the astrocyte and arteriolar smooth muscle. The elevated extracellular [K+] causes hyperpolarization of smooth muscle by activating Na+/K+-ATPase and also by increasing the conductance of inward-rectifying K+ channels. The hyperpolarization reduces Ca++ entry into vascular smooth muscle because the membrane potential is shifted away from the threshold. Hence, the parenchymal arteriole dilates, and blood flow increases.