Nitric Oxide Synthase Inhibitors I: Substrate Analogs and Heme Ligands

Parkinson, John F.

doi:10.1007/978-3-642-57077-3_6

Cited by 1 publication

(1 citation statement)

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“…Inhibitors of NOS activity have also provided evidence for the role of NO in pain sensitization. Yonehara and coworkers ( 1997 ), in a chronic inflammatory pain model, reported a decrease in hyperalgesia after the intravenous administration of the arginine analog N-omega-nitro-L-arginine methyl ester (L-NAME), which inhibits the nNOS and eNOS isoforms (Knowles and Moncada, 1994 ; Parkinson, 2000 ). More recently, however, other groups were also able to show the specific role of iNOS in hyperalgesia by using highly selective inhibitors for this isoform, such as N -(3-[Aminomethyl] benzyl) acetamidine (1400W) (Tang et al, 2007 ) and (S)-2-amino-7-acetamidino-5-thioheptanoic acid (GW274150) (De Alba et al, 2006 ).…”

Section: Hyperalgesia Pain and Nitric Oxidementioning

confidence: 99%

Pain modulation by nitric oxide in the spinal cord.

Freire¹

2009

Front. Neurosci.

104

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Nitric oxide (NO) is a versatile messenger molecule first associated with endothelial relaxing effects. In the central nervous system (CNS), NO synthesis is primarily triggered by activation of N-methyl-D-aspartate (NMDA) receptors and has a Janus face, with both beneficial and harmful properties. There are three isoforms of the NO synthesizing enzyme nitric oxide synthase (NOS): neuronal (nNOS), endothelial (eNOS), and inducible nitric oxide synthase (iNOS), each one involved with specific events in the brain. In the CNS, nNOS is involved with modulation of synaptic transmission through long-term potentiation in several regions, including nociceptive circuits in the spinal cord. Here, we review the role played by NO on central pain sensitization.

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