Signal Transduction of NO

NO-mediated synthesis of cGMP from GTP in the corpus cavernosum that leads to smooth muscle relaxation. Sildenafil potentiates the effects of NO by inhibiting cGMP phosphodiesterase. 

These kinases phosphorylate specific proteins that may be involved in removal or sequestration of Ca or other ions, resulting in physiological stimuli. The physiological actions of cGMP are terminated by its conversion to 5 -GMP by cGMP-phosphodiesterase. Inhibitors of cGMP phosphodiesterase promote the actions of NO. 

The antiaggregability of platelets and the neurotoxicity of NO have been attributed to inhibition of glycolysis by NO. 

The one-carbon carrier N, N -methylenetetrahydrofolate is derived from reactions of the one-carbon pool (Chapter 27). [The term one-carbon pool refers to all single-carbon-containing metabolites (e.g., -CH3, -CHO, NH=C-, etc.) that can be utilized in biosynthetic reactions such as formation of purine and pyrimidine.] These reactions include oxidation of glycine by glycine cleavage enzyme complex (glycine synthase)  

Glycine is also oxidized by D-amino acid oxidase, an FAD protein  

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Action. cAMP is an allosteric effector of protein kinase A (PK-A, [3]). in the inactive state, PK-A is a heterotetramer (C2R2), the catalytic subunits of which (C) are blocked by regulatory units (R autoinhibition). When cAMP binds to the regulatory units, the C units separate from the R units and become enzymatically active. Active PK-A phosphorylates serine and threonine residues of more than 100 different proteins, enzymes, and transcription factors, in addition to cAMP, cCMP also acts as a second messenger, it is involved in sight (see p. 358) and in the signal transduction of NO (see p. 388). 

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