Nitric oxide and the cerebral vascular function.
The presence of a cholinergic vasodilator innervation to cerebral circulation is well established. Despite its high endogenous concentration in cerebral blood vessels, acetylcholine (ACh) is not the transmitter for vasodilation. This finding has led to the discovery that nitric oxide (NO), which is coreleased with ACh and neural peptides such as vasoactive intestinal polypeptide (VIP) from the respective cholinergic-nitrergic (nitric oxidergic) nerves and the VIPergic-nitrergic nerves, is the primary transmitter in relaxing smooth muscle. ACh and VIP act presynaptically to inhibit and facilitate, respectively, the release of NO. Release of NO from cerebral vascular endothelial cells is also well established. A similar system for recycling L-citrulline to L-arginine for synthesizing more NO has been demonstrated in both cerebral perivascular nerves and endothelial cells. Neuronal and endothelial NO appears to play an important role in controlling cerebral vascular tone and circulation in health and disease.
Lee
T J
TJ
Department of Pharmacology, SIU School of Medicine, Springfield, IL 62794-9629, USA. tlee@wpsmtp.siumed.edu
D000818:Animals; D002560:Cerebrovascular Circulation / Q000502:physiology*; D004730:Endothelium, Vascular / Q000737:chemistry; D006801:Humans; D008881:Migraine Disorders / Q000209:etiology; D020078:Neurogenic Inflammation / Q000503:physiopathology; D009569:Nitric Oxide / Q000494:pharmacology* / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects
D009569:Nitric Oxide