Modulation of Opioid Actions by Nitric Oxide Signaling

Author:

Toda Noboru1,Kishioka Shiroh2,Hatano Yoshio3,Toda Hiroshi4,Warner David S.,Warner Mark A.

Affiliation:

1. Professor Emeritus, Shiga University of Medical Science, Shiga, Japan, and Toyama Institute for Cardiovascular Pharmacology Research, Osaka, Japan.

2. Professor of Pharmacology, Department of Pharmacology.

3. Professor of Anesthesiology, Department of Anesthesiology, Wakayama Medical University, Wakayama, Japan.

4. Head of Anesthesiology, Department of Anesthesiology, Kyoto Katsura Hospital, Kyoto, Japan.

Abstract

Nitric oxide (NO) plays pivotal roles in controlling physiological functions, participates in pathophysiological intervention, and is involved in mechanisms underlying beneficial or untoward actions of therapeutic agents. Endogenous nitric oxide is formed by three isoforms of nitric oxide synthase: endothelial, neurogenic and inducible. The former two are constitutively present mainly in the endothelium and nervous system, respectively, and the latter one is induced by lipopolysaccharides or cytokines mainly in mitochondria and glial cells. Constitutively formed nitric oxide modulates the actions of morphine and related analgesics by either enhancing or reducing antinociception. Tolerance to and dependence on morphine or its withdrawal syndrome are likely prevented by nitric oxide synthase inhibition. Information concerning modulation of morphine actions by nitric oxide is undoubtedly useful in establishing new strategies for efficient antinociceptive treatment and for minimizing noxious and unintended reactions.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Anesthesiology and Pain Medicine

Reference164 articles.

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