Key result
Endothelial-derived nitric oxide counterbalances excessive platelet activation through the stimulation of soluble guanylyl cyclase and activation of cyclic AMP and GMP-mediated signaling pathways.
This review summarizes the current understanding of how nitric oxide regulates platelet activation via soluble guanylyl cyclase and cyclic nucleotide signaling pathways.
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.
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Naseem et al. (2010) conducted a review in Platelet activation. Nitric oxide was evaluated. Endothelial-derived nitric oxide counterbalances excessive platelet activation through the stimulation of soluble guanylyl cyclase and activation of cyclic AMP and GMP-mediated signaling pathways.
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