Book contents
- Frontmatter
- Contents
- List of contributors
- Editors' preface
- PART I PHYSIOLOGY
- 1 History of platelets
- 2 Production of platelets
- 3 Morphology and ultrastructure of platelets
- 4 Platelet heterogeneity: physiology and pathological consequences
- 5 Platelet membrane proteins as adhesion receptors
- 6 Dynamics of the platelet cytoskeleton
- 7 Platelet organelles
- 8 Platelet receptors for thrombin
- 9 Platelet receptors: ADP
- 10 Platelet receptors: prostanoids
- 11 Platelet receptors: collagen
- 12 Platelet receptors: von Willebrand factor
- 13 Platelet receptors: fibrinogen
- 14 Platelet signalling: GTP-binding proteins
- 15 Platelet phospholipases A2
- 16 Roles of phospholipase C and phospholipase D in receptor-mediated platelet activation
- 17 Platelet signalling: calcium
- 18 Platelet signalling: protein kinase C
- 19 Platelet signalling: tyrosine kinases
- 20 Platelet signalling: cAMP and cGMP
- 21 Platelet adhesion
- 22 The platelet shape change
- 23 Aggregation
- 24 Amplification loops: release reaction
- 25 Amplification loops: thromboxane generation
- 26 Platelet procoagulant activities: the amplification loops between platelets and the plasmatic clotting system
- 27 Platelets and chemotaxis
- 28 Platelet–leukocyte interactions relevant to vascular damage and thrombosis
- 29 Vascular control of platelet function
- PART II METHODOLOGY
- PART III PATHOLOGY
- PART IV PHARMOLOGY
- PART V THERAPY
- Afterword: Platelets: a personal story
- Index
- Plate section
15 - Platelet phospholipases A2
from PART I - PHYSIOLOGY
Published online by Cambridge University Press: 10 May 2010
- Frontmatter
- Contents
- List of contributors
- Editors' preface
- PART I PHYSIOLOGY
- 1 History of platelets
- 2 Production of platelets
- 3 Morphology and ultrastructure of platelets
- 4 Platelet heterogeneity: physiology and pathological consequences
- 5 Platelet membrane proteins as adhesion receptors
- 6 Dynamics of the platelet cytoskeleton
- 7 Platelet organelles
- 8 Platelet receptors for thrombin
- 9 Platelet receptors: ADP
- 10 Platelet receptors: prostanoids
- 11 Platelet receptors: collagen
- 12 Platelet receptors: von Willebrand factor
- 13 Platelet receptors: fibrinogen
- 14 Platelet signalling: GTP-binding proteins
- 15 Platelet phospholipases A2
- 16 Roles of phospholipase C and phospholipase D in receptor-mediated platelet activation
- 17 Platelet signalling: calcium
- 18 Platelet signalling: protein kinase C
- 19 Platelet signalling: tyrosine kinases
- 20 Platelet signalling: cAMP and cGMP
- 21 Platelet adhesion
- 22 The platelet shape change
- 23 Aggregation
- 24 Amplification loops: release reaction
- 25 Amplification loops: thromboxane generation
- 26 Platelet procoagulant activities: the amplification loops between platelets and the plasmatic clotting system
- 27 Platelets and chemotaxis
- 28 Platelet–leukocyte interactions relevant to vascular damage and thrombosis
- 29 Vascular control of platelet function
- PART II METHODOLOGY
- PART III PATHOLOGY
- PART IV PHARMOLOGY
- PART V THERAPY
- Afterword: Platelets: a personal story
- Index
- Plate section
Summary
Introduction
The major physiological role of platelets is in the cessation of bleeding following damage to the vasculature. Ordinarily, platelets circulate within intact blood vessels in a quiescent state, but undergo extremely rapid and powerful activation upon exposure to the subendothelial matrix leading to formation of a platelet aggregate or vascular plug. This rapid response is achieved by the stimulatory action of a range of diverse agonists including extracellular matrix proteins, e.g. collagen, and products of the coagulation cascade, e.g. thrombin. Activation is reinforced through release of agonists from platelet granules, notably ADP, and liberation of thromboxane A2 (TxA2), the major product of the metabolism of arachidonic acid (AA) in the platelet. The positive feedback action of ADP and TxA2 is of direct clinical relevance. The Antiplatelet Trialists' Collaboration published a summary of 20 randomized trials in 1988, concluding that antiplatelet therapy significantly reduces (by ∼ 25%) the risk of cardiovascular death, non-fatal myocardial infarction and nonfatal stroke in patients with unstable angina or a past history of heart attack, transient ischemic attack, or stroke. A follow-up report by the same group, confirmed the efficacy of platelet inhibition in a broader spectrum of pathological conditions. More recently, the CAPRIE study has shown that the ADP receptor antagonist, clopidogrel, and aspirin have a similar therapeutic benefit in individuals with a history of thrombotic disease. Aspirin, however, remains the drug of choice in the majority of cases primarily for reasons of cost.
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- Platelets in Thrombotic and Non-Thrombotic DisordersPathophysiology, Pharmacology and Therapeutics, pp. 221 - 237Publisher: Cambridge University PressPrint publication year: 2002
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