D Salvemini et al.
The Journal of clinical investigation, 97(11), 2562-2568 (1996-06-01)
We have evaluated the contributions of nitric oxide (NO) and prostacyclin (PGI2) in the in vivo antiplatelet effects of clinically useful nitrovasodilators. In rats, intravenous infusion of three NO donors, glyceryl trinitrate, sodium nitroprusside, or 3'-morpholinosydnonimine, the stable metabolite of...
M Maccarrone et al.
Biochemical and biophysical research communications, 219(1), 128-133 (1996-02-06)
The nitric oxide (N0-releasing agents sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) inhibit dioxygenase activity of lipoxygenase in human platelets and human CHP100 neuroblastoma cells, leading the latter to necrosis. The effect of both NO-donors on the dioxygenase reaction was investigated...
Journal of Cardiovascular Pharmacology, 17, S25-S25 (1991)
B Brüne et al.
The Journal of biological chemistry, 264(15), 8455-8458 (1989-05-25)
Sodium nitroprusside is a vasodilator and an inhibitor of platelet activation. It is thought that these effects are mediated by the spontaneous release of nitric oxide and stimulation of cytosolic guanylate cyclase. We have found that sodium nitroprusside (5-200 microM)...
F J Azula et al.
Molecular pharmacology, 50(2), 367-379 (1996-08-01)
Different drugs that elevate the cGMP levels inhibit the agonist-induced platelet activation. The mechanisms of action of cGMP probably include inhibition of both phospholipase C and the increase in intracellular Ca2+ concentration, and these effects seem to be mediated by...