Local chemical, neural, and humoral regulation of cerebrovascular resistance vessels.

Local chemical factors, such as H+, K+, Ca2+, adenosine, and osmolarity, affect cerebral resistance vessels. Their participation in the regulation of cerebral blood flow is suggested by changes in their concentration in the interstitial space during increased neuronal activity, strong hypoxia, and transient of incomplete ischemia. Such changes are not observed during autoregulation. Possible interactions between several factors must be considered when estimating their role. Autonomic nerves innervating cerebral vessels include: sympathetic nerves releasing the constrictor transmitter noradrenaline; parasympathetic nerves (liberating the dilator transmitter acetylcholine) and other dilator fibers (containing either serotonin, substance P, or vasoactive intestinal polypeptide). Participation of these systems in the adjustment of cerebral blood flow is still a matter of discussion, except for the protective effect of sympathetic nerves on the upper limit of autoregulation and on the blood--brain barrier. Humoral compounds, generated and released within the brain, which can affect cerebral blood flow include: histamine, bradykinin, and prostaglandins. Histamine, bradykinin, prostaglandin E2, and prostacyclin dilate cerebral arteries in situ, while prostaglandin F2 alpha reduces cerebral blood flow. Histamine and bradykinin alter the permeability of the blood--brain barrier and might be involved in pathological events, such as edema.