Inhibition of Nitric Oxide Biosynthesis Promotes P-selectin Expression in Platelets
Key result
Inhibition of NO synthesis by L-NAME significantly increased P-selectin expression on platelets via PKC activation, an effect attenuated by NO donors and PKC inhibitors.
Population
Platelets and endothelial cells (coronary artery endothelium)
Comparison
NO synthase inhibitor NG-nitro-L-arginine methyl… vs Control, or co-incubation with PKC inhibitor…
Design
Preclinical
Follow-up
10 minutes
Authors
Discussion
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Member takes
Implication
NO-PKC pathway may modulate platelet activation; hypothesis-generating for antithrombotic targets, pending human studies.
Structured PICO
P
Population
Platelets and endothelial cells (coronary artery endothelium)
I
Intervention
NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), phorbol 12-myristate 13-acetate (PMA), or thrombin (10-minute incubation)
C
Comparator
Control, or co-incubation with PKC inhibitor UCN-01, L-arginine, 8-bromo-cGMP, sodium nitroprusside (SNP), or anti-P-selectin antibodies
O
Outcome
P-selectin expression on platelets and PKC activity of platelet membranessurrogate
Inhibition of nitric oxide synthesis induces rapid P-selectin expression in platelets and endothelial cells, partially mediated by protein kinase C activation.
Cite This Study
Murohara et al. (1995) studied this question. L-NAME (NO synthase inhibitor) was evaluated on P-selectin expression on platelets and PKC activity. Inhibition of NO synthesis by L-NAME significantly increased P-selectin expression on platelets via PKC activation, an effect attenuated by NO donors and PKC inhibitors.