Haloperidol inhibits neuronal nitric oxide synthase activity by preventing electron transfer
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Updated: Nov 3, 2026

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
Published on: March 16, 2017
K Iwahashi1, H Yoneyama, T Ohnishi
1Department of Neuropsychiatry, University Hospital, Kagawa Medical School, Japan.
Abstract:
The effect of a neuroleptic, haloperidol (HP), on nitric oxide formation catalyzed by neuronal nitric oxide synthase (n-NOS) in the porcine brain was investigated. HP inhibited n-NOS activity noncompetitively versus L-arginine as a substrate, decreasing the maximal velocity (Ki value for HP = 31 microM). HP also inhibited the CaM-dependent NADPH consumption by n-NOS (IC50 = 221 microM). These data demonstrate the possibility that HP may mediate some neuronal functions through inhibiting NO release by preventing either the electron transfer through n-NOS or the formation of the activated reduced species of oxygen necessary for the formation of citrulline. And an interaction of HP with CaM may possibly affect the consumption of NADPH and n-NOS enzyme activity.
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meta-Directing Deactivators: –NO2, –CN, –CHO, –⁠CO2R, –COR, –CO2H