Background: Organic “nitro” compounds such as nitroglycerine, isosorbide dinitrate are
useful in the control of chest pain in acute coronary syndrome. But the mechanism of it in pain
regulation remains speculative. Here, increase of NO production was investigated by the possible
regulation of constitutive nitric oxide synthase (cNOS) function from goat arterial endothelial cells.
This protein was purified and sequence wise characterized as protein disulfide isomerase (PDI) in
response to different nitro compounds.
Method: The NO generating protein was isolated from arterial endothelial cells and prepared to
homogeneity. NO was determined by methemoglobin method. Protein sequence was analyzed by
Results: A protein of Mr. ~57 kDa was isolated and found to be activated by not only “nitro” compounds
but also by acetyl salicylic acid, insulin and glucose. The global BLAST of the protein sequence
showed a significant alignment of the protein sequence with PDI. This protein trivially
called pluri activator stimulated endothelial NOS (PLASENOS). The enzyme was stimulated by the
above-mentioned activators in the presence of Ca2+. Lineweaver-Burk plot of this NOS like activities
were demonstrated with its specific substrate l-arginine as Vmax = 5(nmol NO/mg of protein/hr)
and Km≈ 0.5µM by the above activators. The enzyme activity was inhibited by the l-NAME, the
specific inhibitor of NOS.
Conclusion: The organic nitro compounds, acetyl salicylic acid, insulin and glucose were found to
activate PLASENOS in the arterial endothelial cells for a continuous supply of NO to control the
chest pain in acute coronary syndrome.