Good question. I saw a lot of conflicting info on NO too. I never took time to figure it out though. I think this is might explain why it is bad for pwms.
The Good (in normal people)http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533368/
NO synthesis has also clearly been shown to have a beneficial role in regulating organ perfusion and mediating cytotoxicity.
There's probably a lot more good but I'm too lazy to find it all.
The Bad (in pwms)
Using triple-labeled fluorescent immunocytochemistry, we also show that Nav1.6, which is known to produce a persistent sodium current, and the Na+/Ca2+ exchanger, which can be driven by persistent sodium current to import damaging levels of calcium into axons, are colocalized with β-amyloid precursor protein, a marker of axonal injury, in acute MS lesions. Our results demonstrate the molecular identities of the sodium channels expressed along demyelinated and degenerating axons in MS and suggest that coexpression of Nav1.6 and Na+/Ca2+ exchanger is associated with axonal degeneration in MS.http://cdn.intechopen.com/pdfs/34158/In ... e_drug.pdf
Inhibition of L-type Ca2+ channels (vascular smooth muscle, in vitro); inhibition of N-type Ca2+ channels (sympathetic neuron, in vitro)http://www.ingentaconnect.com/content/m ... 3/art00015
1) Cardiovascular action
Vascular relaxation (in vitro); hypotensive action (in vivo)
2) Anti-sympathetic action
Decrease of catecholamine release, tissue (kidney) norepinephrine level, (in vitro, in vivo); inhibition of sympathetic tachycardia and cold stress-induced vasoconstriction (in vivo); decrease in plasma/urinary norepinephrine, muscle sympathetic nerve activity, low frequency/high frequency ratio (LF/HF ratio), and plasma level of ß-thromboglobulin (clinical)
3) Suppression of renin- angiotensin-aldosterone system
Decrease in plasma level of angiotensin II and aldosterone (in vivo, clinical); inhibition of aldosterone production (adrenocortical cells, in vitro); inhibition of reflex aldosterone production, and angiotensin II-renin feedback (in vivo)
Inhibition of NADPH oxidase-derived superoxide production (kidney, in vivo)
Peroxynitrite, a reactive oxidant formed by the reaction of nitric oxide with superoxide at sites of inflammation in multiple sclerosis (MS), is capable of damaging tissues and cells.
We have elevated levels of ca2 in MS. If you inhibit ca2 channels, production of superoxide is decreased...which would mean that ca2 is involved in superoxide production and likely causes increased levels of superoxide in pwms. If you add NO, superoxide can react with it creating peroxynitrite, which damages cells and tissues. Pwms have low levels of uric acid which can be attributed to it's "work" in scavenging peroxynitrite. So, I think ultimately, NO is bad for pwms...it helps make more brain eaters.