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Nitric Oxide – A Novel Autonomic Neurotransmitter

Nitric Oxide – A Novel Autonomic Neurotransmitter 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, Ca<sup>2+</sup>/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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cells Tissues Organs Karger

Nitric Oxide – A Novel Autonomic Neurotransmitter

Cells Tissues Organs , Volume 150 (1): 9 – Jan 1, 1994

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Publisher
Karger
Copyright
© 1994 S. Karger AG, Basel
ISSN
1422-6405
eISSN
1422-6421
DOI
10.1159/000147598
Publisher site
See Article on Publisher Site

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, Ca<sup>2+</sup>/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.

Journal

Cells Tissues OrgansKarger

Published: Jan 1, 1994

Keywords: Autonomic nervous system; NADPH-diaphorase; Neurotransmission; Nitric oxide; Nitric oxide synthase

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