Nitric Oxide – A Novel Autonomic Neurotransmitter

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Abstract
Considerable evidence suggests that nitric oxide (NO) acts as a nonadrenergic noncholinergic (NANC) transmitter at autonomic neuroeffector junctions. NO is generated enzymatically from L-arginine by a constitutive, cytosolic, Ca2+/calmodulin-activated NO synthase (NOS): NADPH- and tetrahydrobiopterin-dependent cytochrome P-450-type hemoprotein. Electrophysiological and pharmacological data indicate that NO fulfils most of the criteria for a neurotransmitter. It is released from axon terminals when invaded by action potentials and mimics the effect of nerve stimulation. The changes in the mechanical and/or electrical activity of smooth muscle preparations in response to transmural stimulation of NANC nerves are antagonized by inhibitors of NO synthesis or oxyhemoglobin, an NO scavenger. NO acts principally by stimulating soluble guanylate cyclase. Studies on the histochemical localization of NOS point to the involvement of the neural L-arginine-NO pathway in the regulation of vascular tone and of several aspects of respiratory, gastrointestinal, and genitourinary tract functions.

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