The role of nitric oxide and cGMP in platelet adhesion to vascular endothelium
MW Radomski, RMJ Palmer, S Moncada - Biochemical and biophysical …, 1987 - Elsevier
MW Radomski, RMJ Palmer, S Moncada
Biochemical and biophysical research communications, 1987•ElsevierThe inhibition of platelet adhesion by nitric oxide (NO) and prostacyclin and their mechanism
of action was studied. Platelet adhesion to collagen fibrils and endothelial cell matrix was
inhibited completely by NO but only partially by prostacyclin. Adhesion of platelets to
endothelial cell monolayers was inhibited by bradykinin. This effect of bradykinin was
unaffected by aspirin, and was accounted for by the amounts of NO released by the
endothelial cells. Inhibition of platelet adhesion by NO and prostacyclin was potentiated by …
of action was studied. Platelet adhesion to collagen fibrils and endothelial cell matrix was
inhibited completely by NO but only partially by prostacyclin. Adhesion of platelets to
endothelial cell monolayers was inhibited by bradykinin. This effect of bradykinin was
unaffected by aspirin, and was accounted for by the amounts of NO released by the
endothelial cells. Inhibition of platelet adhesion by NO and prostacyclin was potentiated by …
Summary
The inhibition of platelet adhesion by nitric oxide (NO) and prostacyclin and their mechanism of action was studied. Platelet adhesion to collagen fibrils and endothelial cell matrix was inhibited completely by NO but only partially by prostacyclin. Adhesion of platelets to endothelial cell monolayers was inhibited by bradykinin. This effect of bradykinin was unaffected by aspirin, and was accounted for by the amounts of NO released by the endothelial cells. Inhibition of platelet adhesion by NO and prostacyclin was potentiated by selective inhibitors of cGMP phosphodiesterase, but not of cAMP phosphodiesterase, indicating that elevation of cGMP regulates platelet adhesion.
Elsevier