Table 1.
The main stimuli and pathways involved in nitric oxide (NO) and carbon monoxide (CO)-induced effects on platelets. Abbreviations: eNOS endothelial nitric oxide synthase; iNOS inducible nitric oxide synthase; HO-1 heme oxygenase 1; cGMP cyclic guanosine monophosphate; HNO Nitroxyl; PKG protein kinase cGMP-dependent; IL-1β interleukin-1 β; PKC protein kinase C; ONOO− peroxynitrite.
| Gas | Stimuli | Production | Main Pathway | Effect(s) |
|---|---|---|---|---|
| NO | Shear stress, VEGF, insulin | Endothelial cells (eNOS) |
NO/cGMP/PKG | Vasodilation |
| [Ca]i increase, interaction protein (HSP70, HSP90, caveolin), insulin, β2 stimulation, acetylsalicylic acid, adenosine, and forskolin |
Platelets (eNOS) |
NO/cGMP/PKG | Reduction of adhesion, activation, and aggregation |
|
| Inflammation | Platelets iNOS |
NO/cGMP/PKG | Increased production of NO correlates with IL-1β |
|
| Conditioning ischemia | Cardiac cells (eNOS or iNOS) |
NO/cGMP/PKG S-nitrosylation |
Cardioprotection | |
| HNO | Conditioning ischemia | Cardiac cells (eNOS?) | PKCε translocation to the mitochondria |
Cardioprotection |
| ONOO− | Metabolic diseases | NO + O2− | nitration carbonylation and peroxidation |
Alteration of haemostatic functions |
| CO | Hemin and sodium arsenite | Platelet HO-1 |
cGMP/PKG | Reduction of aggregation and release of ADP and 5-HT |
| Conditioning ischemia | Cardiac cells HO-1 |
Opening of KATP channel and closure of the MPTP. |
Cardioprotection |