Platelet-vessel wall interaction: role of nitric oxide, prostaglandins and endothelins

Platelets can interact with the blood vessel wall in numerous ways. By releasing vasoactive substances such as adenosine tri- and diphosphate as well as serotonin, platelets can stimulate the formation of nitric oxide and prostacyclin within endothelial cells. Under physiological conditions, this may provide an important protective mechanism providing platelet inhibition and increased local blood flow at sites of platelet activation. In addition, platelets also can stimulate the formation of the vasoconstrictor peptide endothelin-1 within endothelial cells. On the other hand, platelet-derived substances such as thromboxane and serotonin can activate vascular smooth muscle cells and cause profound vasoconstriction. Platelet-vessel wall interaction is normally very low due to protective mechanisms. In disease states, however, endothelial dysfunction increases platelet-vessel wall interaction. Low-density lipoproteins markedly reduced endothelium-dependent relaxations to aggregating platelets and serotonin. Even more marked changes in endothelial function occur in atherosclerosis. These functional alterations of platelet-vessel wall interaction may play an important role in the pathogenesis of cardiovascular disease.