Mechanisms of stimulus-response coupling in platelets

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Mechanisms of stimulus-response coupling in platelets

edited by J. Westwick ... [et al.]

（Advances in experimental medicine and biology, v. 192）

Plenum Press, c1985

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"Proceedings of a symposium ... held September 27-28, 1984, in De Crespigny Park, London, England"--T.p. verso

Includes bibliographies and index

内容説明・目次

内容説明

Since its inception the research area of platelet pharmacology has always been a vigorous one and it is a characteristic that new approaches to the understanding of platelet function are rapidly and thoroughly investigated. The intensity of this activity is attri- butable, probably, to an appreciation by research workers in the field that a satisfactory therapeutic control of platelet function has yet to be realized. Also that if and when this problem of con- trolling platelet function is achieved the benefits to clinical medicine will be immense since platelets are known to be involved in a multiplicity of events coupled within the haemostatic mechanisms and inflammatory responses. Aberrations in the behaviour of plate- lets is part of the aetiology of atherosclerosis, myocardial and cerebral infarction and thrombosis. At this point in time, research in platelet function is in a particularly rapid state of flux. The recent findings of research workers active in the field and also workers investigating mechan- isms of stimulus response coupling in other cells, have provided interesting insights into the generality of mechanisms involved in the function of responsive cells. One may itemize these developments as the area of cell receptor/ligand interaction, induction of cell- ular response by protein phosphorylation and calcium flux. The mech- anism of these latter events occurs through the activity of phospho- lipase generating transient intermediates. These intermediates may act as ionophores or enzyme activators or may, in the case of eico- sanoids, reinforce and make irreversible the cellular response.

目次

  • Platelet Receptors.- Structure and Organisation of Platelet Membranes.- Platlet Receptors for Thrombin.- Characterisation of ADP Receptors.- Fibrinogen and Platelet Function.- Characterisation of Factor VIII Receptors.- Characterization of Thromboxane Receptors in Human Platelets.- Specific Binding of [3H]-1-O-Octadecyl PAF-Acether to Washed Human Platelets.- Characterisation of Human Platelet Adrenoceptors.- Specificity Between the Anti-Aggregatory Actions of Prostacyclin, Prostaglandin E1 and D2 on Platelets.- Control of Calcium Mobilization.- Agonist-Induced Inositol Phospholipid Metabolism and Ca++ Flux in Human Platelet Activation.- Control and Interrelation of Aggregation and Secretion
  • The Roles of Ca2+, Diacylglycerol and Thromboxane with Particular Reference to ADP Stimulation.- Measurement of Intracellular Platelet Calcium with Aequorin and Quin 2.- Permeabilised Platelets and Exocytosis.- Platelet Membranes, Eicosanoid Biosynthesis and Putative Endogenous Calcium Ionophores.- Hydrolysis of Cytoskeletal Proteins by The Ca2+-Dependent Protease During Platelet Activation.- Phosphorylation of Platelet Proteins and Nucleotide Metabolism.- Energy Requirements of Stimulus-Response Coupling.- Platelet Protein Phosphorylation.- Protein Kinase C and Granule Release in Human Platelets.- Receptor-Effector Coupling in Platelets: Roles of Guanine Nucleotides.- Products of Phospholipid Metabolism.- Regulation of Platelet Phospholipid Metabolism.- Role of Thromboxane A2.- Role of PAF-Acether and Related Ether-Lipid Metabolism in Platelets.- Role of Lipoxygenase Products in Platelet Function: Relation to Fatty Acid Modified Phospholipids.- Biological Actions of Prostacyclin and Its Pharmacological use in Platelet Studies.- Functional Platelet Responses.- Development of Procoagulant Binding Sites on the Platelet Surface.- Mechanism of Inhibition of Platelet Coagulant Activity.- Platelet Interaction with the Contact System of Coagulation.- Adenosine Diphosphate as a Mediator of Platelet Aggregation in vivo.- Molecular Mechanism of Platelet Adhesion.- Endothelium as a Modulator of Platelet Reactivity.- Platelet-Derived Heparin Neutralizing Proteins.

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