Potential cardiodepressant effects of NO |
(1) Alterations in protein kinase activity and then L type calcium channel |
(2) Decrease in the myofibril response to calcium |
(3) Decreased cAMP via phosphodiesterase |
(4) Direct inhibition of mitochondrial respiration and therefore adenosine triphosphate production within the myocardium |
(5) Stimulation of cellular damage following binding with reactive oxygen species to form peroxynitrite |
(6) Triggering of apoptosis in cardiomyocytes |
Potential cardioprotective effects of NO |
(1) Increased myocardial perfusion due to vasodilatory effect |
(2) Free radical scavenger reducing ischaemia reperfusion injury via: |
–inhibition of platelet aggregation |
–inhibition of leucocyte adhesion to endothelial cells |
–stabilisation of cell membranes |
(3) Mediation of ventricular dilatation allowing utilisation of Frank-Starling mechanism |
(4) Antiarrhythmic properties of NO |
(5) Macrophage activation leading to bacterial lysis |