Yes, of course: Sodium nitroprusside is NO-releasing and has been extensively used in intensive care medicine to control extreme hypertension by intravenous application (along with release of free cyanide). For cell culture experiments I would recommend SNAP, Spermine-NONOATE etc. These compounds will directly release NO. Just determine the desired half-life for your experiments and chose one of the compounds (There are dozens available).

NONOates are the easiest to work with in the lab. Quite stable at high pH and low temperature, so you can make stocks and "trigger" NO release by diluting into a warm physiological buffer. As noted above, there are many compounds with various half-lives of release available.

I recommend looking at the Keefer website:

http://star.ncifcrf.gov/nitricoxide/default.aspx

But beware, some of the byproducts can be toxic!

For example, we used DPTA/NO for some in vivo experiments and noticed the parent compound, DPTA, was toxic. So be sure and have appropriate controls.

Dear Swami.

Nitroglycerine is probably the most well known NO releasing drug as it has been used for over 100 years to treat angina pectoris etc.  The other two major clases are diazenium diolates (NONOates as described above) and S-nitrosothiols. You can also make your own NONOates by exposing suitable amines to nitric oxide gas, e.g see attached

Best regards, Deon

Article Nitric Oxide Release from Polydimethylsiloxane-based Polyurethanes

It really depends from your needs and intended use,

the above mentioned NONOates or diazenium diolates have half lives ranging from milliseconds to hours. (See the work of Larry K. Keefer as an example)

But my suggestion as additional hint is isosorbide mononitrate or isosorbide dinitrate, that is used for angina, but be careful that the mechanism of release is different from that of nitroglycerin (spontaneous + glutathion mediated) or NONOates (spontaneous)

I would echo all the above statements. The choice of NO donor or releasing agents are dependent on your experimental set up. For me NONOates are good as there is known a stochemetric release of NO and half life depending on the NONOate you use, meaning  you have better control of the amount and rate of release of NO. The down side is that release is spontaneous in aqueous solution and while this can be controlled by keeping stocks on ice or in high pH you may find it best to make new dilutions for each experimental group as dilutions can go "off" very quickly. This is particularly true if you are doing isolated organ experiments with for example arterial or smooth muscle preps; here you will want a NONOate with a relatively short half life to provide rapid responses. 

Another reason I prefer NONOates is they are "pure" NO donors; it is worth noting that other NO donors such as SNP are thought to release reactive nitrogen species other than NO, similarly agents such as Nicorandil have other mechanisms of action which may have effects that produce responses similar to what you would expect with NO (e.g. Smooth muscle relaxation due to opening KATP) and thus in certain experimental systems may confuse your analysis.

Sodium Nitroprissude (SNP) has been clinicaly used for over a century. As far as I know, these days it becomes less common, and is given for imergency cases mostly. 

NONOates, Nitroglycerine are not the direct inducers of NO in endothelial cells via receptor interaction. Estrogen activates via estrogen receptor. We can send if you need

Muscle dystrophies are heritable diseases that result from defects in muscle proteins. These defects cause progressive muscle damage, and in the most severe cases, can lead to paralysis and death, due to heart and/or breathing difficulties.

Nitric oxide is a compound that is made by the body, and normally functions to activate cells surrounding muscle fibres, called satellite cells. Satellite cells have the ability to make new muscle fibres to repair muscle damage from normal daily activity. However, nitric oxide is found to be misplaced and thus not active in people with muscular dystrophy. As a result, the satellite cells become exhausted, and eventually lose their ability to make new muscle fibres. This leads to breakdown of muscle fibres, and inflammation. The deteriorating muscle becomes replaced with scar tissue. Eventually, symptoms worsen leading to muscle weakness and muscle breakdown.

To counteract these effects, previous studies have shown that a drug capable of releasing nitric oxide within the muscle tissue can reduce muscle breakdown. Administration of an anti-inflammatory drug, such as ibuprofen, reduces inflammation. Together, the two drugs are known to preserve the activity of satellite cells to make new muscle fibres that restore the health of the muscle.

This study is to test a new drug, called NCX 320 that can simultaneously release both nitric oxide, and ibuprofen, in mice with muscular dystrophy. The effect of the drug in reducing muscle breakdown, inflammation, and improving satellite cell activity can be evaluated.

Please contact Nicox Research Institute for recent updates on the subject, there are other drugs currently in development for Duchenne.

If you need contact details please contact me privately.

thanks 

I know this is a very old thread, but I have a question regarding DPTA NONOates. Anyone has used it for bacteria? did you observe any toxic effects on bacteria of DPTA? I am asking this here since Peter Sobolewski mentioned it. Can you elaborate your experience Peter Sobolewski

We were using DPTA/NO as a NO donor drug in a mouse malaria model, as a way of restoring NO bioavailability. The results were published here:

Article Low nitric oxide bioavailability contributes to the genesis ...

The results presented were with a DPTA/NO dose of 1 mg twice daily. When we increased the dose to 3 mg twice daily we observed hind limb paralysis in the mice, which we attributed to the parent compound DPTA.

thanks a lot