No Nitric Oxide for HO-1 from Sodium Nitroprusside

Abstract

Nitric oxide (NO) and NO donors were among the first reported inducers of the tissue-protective protein heme oxygenase-1 (HO-1) with a potential for eventual use in humans. Besides other clinically established NO releasing drugs, sodium nitroprusside (SNP) has frequently been employed as an experimental tool to explore effects of NO on HO-1 and other biological targets. In this issue of Molecular Pharmacology, Kim et al. (p. 1633) demonstrate that the effects of SNP on expression of HO-1 are mainly due to free iron released from SNP in aqueous solution, whereas NO plays a negligible role, if any, as the mediator of response to SNP. Downstream effects of iron, after being dissociated from SNP, include increases in intracellular cAMP that are causally linked to subsequent phosphorylation of specific MAPK targets and enhanced HO-1 protein levels.

Identification of Nitric Oxide as an Endogenous Inhibitor of 26S Proteasomes in Vascular Endothelial Cells

“…2A), suggesting SNP negatively regulated the association between 19S and 20S sub-complexes. To exclude the possibility that SNP might act on NO-independent manner as reported in macrophages [54], [55], we repeated the experiment with DETA-NONOate. As depicted, DETA-NONOate recapitulated the effects of SNP (Fig.…”

Nitric oxide modulates the influx of extracellular Ca2+ and actin filament organization during cell wall construction in Pinus bungeana pollen tubes

“…The involvement of NO in tip growth has been investigated using pharmacological agents to alter endogenous NO concentrations (Prado et al ., 2004; He et al ., 2007; Salmi et al ., 2007). In the present study, SNAP was selected as the NO donor instead of sodium nitroprusside (SNP), because application of SNP as an NO donor has side effects (Planchet & Kaiser, 2006; Schröder, 2006). The results showed that endogenously generated NO was almost absent at the tip of control pollen tubes but was at higher concentrations behind the clear zone of the tip region, which are in accordance with the findings of Prado et al .…”

Baroreceptor stimulation enhanced nitric oxide vasodilator responsiveness, a new aspect of baroreflex physiology

“…To test the hypothesis that the underlying mechanism lies in baroreflex modulatory effect on NOdependent vasodilation the magnitude of the cutaneous vasodilator response to sodium nitroprusside, a spontaneous NO donor (Schröder, 2006), was determined in relation to an increase in baroreflex sensitivity generated by carotid baroreceptor magnetic activation.…”