Global Journal of Science Frontier Research, G: Bio-Tech & Genetics, Volume 22 Issue 2

Figure 2: Phospholipids surface, platelet and endothelium, consist of extrinsic, intrinsic and common pathways results in formation of stable fibrin clot i. Resting platelets Platelets act as a vascular guard, monitoring the integrity of the endothelium; in the absence of injury, resting platelets circulate freely. Chemical mediators, such as prostacyclin and nitric oxide, are synthesized by intact endothelial cells and act as platelet aggregation inhibitors. Prostacyclin works by integration with platelet membrane receptors coupled to the synthesis of cAMP → increased cAMPis associated with the decrease of intracellular Ca +2 , which leads to inhibition of platelet aggregation. Damaged endothelial cells synthesize lower prostacyclin; thus the binding of prostacyclin to platelet receptors is decreased, leading to lower levels of intracellular cAMP, which leads to platelet aggregation. ii. Platelet adhesion When the endothelium is injured, platelets adhere to and cover the exposed collagen of the sub- endothelium iii. Platelet activation Receptors on the surface of the adhering platelets are activated → morphologic changes in theplatelets → release of platelet granules containing chemical mediators, such as adenosine diphosphate (ADP), thromboxane A2, serotonin, platelet activation factor and thrombin. 1. Platelet aggregation The increase in the cytosolic Ca +2 accompanying activation leads to: • The release of platelet granules containing mediators, such as ADP and serotonin, that activate other platelets • Activation of thromboxane A2 synthesis • Activation of glycoprotein GP;IIb/IIIa receptors that bind fibrinogen and ultimately regulate platelet- platelet interaction and thrombus formation © 2022 Global Journals 1 Year 2022 2 Global Journal of Science Frontier Research Volume XXII Issue ersion I VII ( G ) Modulation of Warfarin Sodium into Warfarin Potassium for Patients with Hypertension