Nitric oxide at a glance.
In healthy blood vessels excessive platelet activation is counterbalanced by negative signalling cascades that modulate activation. This is achieved primarily through endothelial-derived nitric oxide (NO) and prostacyclin (PGI2). The biological effects of NO are mediated through stimulation soluble guanylyl cyclase (sGC) activation of cyclic AMP and GMP-mediated signalling pathways. In the present review examine our current understanding of NO-mediated regulation of platelets and highlight key issues that remain unresolved.
Hull York Medical School, University of Hull, Hull, Yorkshire, UK. khalid.naseem@hyms.ac.uk
Khalid M
KM
Naseem
Wayne
W
Roberts
D001792:Blood Platelets / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D015398:Signal Transduction
D009569:Nitric Oxide; D000242:Cyclic AMP; D006152:Cyclic GMP