title: Increased number of thromboxane A2-prostaglandin H2 platelet receptors in active unstable angina and causative role of enhanced thrombin formation.
abstract: The current study was designed to investigate the number and affinity of platelet thromboxane A2/prostaglandin H2 (TxA2/PGH2) receptors in patients with unstable angina and, if any, the role played by the increased thrombin formation that is a common finding in these patients. Measurements taken during active unstable angina but not those taken during inactive angina showed an increase number (p < 0.001), without changes in affinity, of platelet TxA2/PGH2 receptors, evaluated as the binding capacity of iodine 125-PTA-OH, a stable TxA2 analogue. Moreover patients with active angina had higher plasma concentrations of fibrinopeptide A (FPA) (p < 0.0001), which were significantly related to the number of platelet TxA2/PGH2 receptors (r = 0.76; p < 0.01). Heparin infusion but not aspirin treatment promptly normalized the number of TxA2/PGH2 receptors and significantly reduced plasma FPA concentrations. In an in-vitro study thrombin in a concentration similar to that found in vivo significantly increased the number of platelet TxA2/PGH2 receptors (p < 0.01), whereas heparin did not affect TxA2/PGH2 receptors. These results have important therapeutic implications and indicate the preferential use of heparin rather than aspirin during the acute phase of unstable angina.
authors.affiliation: Clinica Medica I, Center for Heart and Thrombosis Research, University of Florence, Italy.
authors.forename: P A
authors.initials: PA
authors.lastname: Modesti
authors.forename: A
authors.initials: A
authors.lastname: Colella
authors.forename: I
authors.initials: I
authors.lastname: Cecioni
authors.forename: A
authors.initials: A
authors.lastname: Costoli
authors.forename: D
authors.initials: D
authors.lastname: Biagini
authors.forename: A
authors.initials: A
authors.lastname: Migliorini
authors.forename: G G
authors.initials: GG
authors.lastname: Neri Serneri
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood; D000789:Angina, Unstable / Q000097:blood* / Q000188:drug therapy / Q000209:etiology; D001241:Aspirin / Q000008:administration & dosage; D001792:Blood Platelets / Q000737:chemistry* / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005344:Fibrinopeptide A / Q000032:analysis / Q000187:drug effects; D006493:Heparin / Q000008:administration & dosage; D006801:Humans; D008875:Middle Aged; D005082:Physical Exertion; D015539:Platelet Activation; D011463:Prostaglandins H / Q000097:blood*; D011869:Radioligand Assay; D011982:Receptors, Prostaglandin / Q000032:analysis* / Q000187:drug effects; D017482:Receptors, Thromboxane / Q000032:analysis* / Q000187:drug effects; D044244:Receptors, Thromboxane A2, Prostaglandin H2; D013917:Thrombin / Q000096:biosynthesis* / Q000494:pharmacology; D013928:Thromboxane A2 / Q000097:blood*
chemical_list: D011463:Prostaglandins H; D011982:Receptors, Prostaglandin; D017482:Receptors, Thromboxane; D044244:Receptors, Thromboxane A2, Prostaglandin H2; D005344:Fibrinopeptide A; D013928:Thromboxane A2; D006493:Heparin; D013917:Thrombin; D001241:Aspirin