Literature DB >> 1273582

Sodium arachidonate can induce platelet shape change and aggregation which are independent of the release reaction.

R L Kinlough-Rathbone, H J Reimers, J F Mustard, M A Packham.   

Abstract

Sodium arachidonate causes shape change and aggregation of rabbit or human platelets that have been washed and then degranulated by treatment with thrombin. Since these platelets do not contain releasable adenosine diphosphate (ADP) and the aggregation is not inhibited by the creatine phosphate-creatine phosphokinase system, sodium arachidonate must be able to cause aggregation that is independent of the release of ADP. Since aggregation of these platelets induced by sodium arachidonate is inhibited by acetylsalicylic acid or indomethacin, it seems likely that products (such as prostaglandin G2) formed from sodium arachidonate are responsible for aggregation. Thus, sodium arachidonate-induced shape change and aggregation of platelets may be caused (i) by the release of ADP by products of sodium arachidonate metabolism and (ii) directly by the products of sodium arachidonate metabolism, independently of released ADP.

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Year:  1976        PMID: 1273582     DOI: 10.1126/science.1273582

Source DB:  PubMed          Journal:  Science        ISSN: 0036-8075            Impact factor:   47.728


  11 in total

1.  Rapid inactivation of cyclooxygenase activity after stimulation of intact platelets.

Authors:  E G Lapetina; P Cuatrecasas
Journal:  Proc Natl Acad Sci U S A       Date:  1979-01       Impact factor: 11.205

2.  In vivo platelet aggregation in the rat: dependence on extracellular divalent cation and inhibition by nonsteroidal anti-inflammatory drugs.

Authors:  G Mallarkey; G M Smith
Journal:  Br J Pharmacol       Date:  1984-01       Impact factor: 8.739

3.  Neutrophil aggregation and degranulation. Effect of arachidonic acid.

Authors:  J T O'Flaherty; H J Showell; E L Becker; P A Ward
Journal:  Am J Pathol       Date:  1979-05       Impact factor: 4.307

4.  Effects of fenflumizole on aggregation ex vivo of human platelets and formation of thromboxane B2 and 6-keto-prostaglandin-F1 alpha.

Authors:  E Vinge; T Corell; K E Andersson
Journal:  Eur J Clin Pharmacol       Date:  1984       Impact factor: 2.953

5.  Role of calmodulin in platelet aggregation. Structure-activity relationship of calmodulin antagonists.

Authors:  M Nishikawa; H Hidaka
Journal:  J Clin Invest       Date:  1982-06       Impact factor: 14.808

6.  Reversal of shortened platelet survival in rats by the antifibrinolytic agent, epsilon aminocaproic acid.

Authors:  P D Winocour; R L Kinlough-Rathbone; M Richardson; J F Mustard
Journal:  J Clin Invest       Date:  1983-01       Impact factor: 14.808

7.  The P2Y12 antagonists, 2-methylthioadenosine 5'-monophosphate triethylammonium salt and cangrelor (ARC69931MX), can inhibit human platelet aggregation through a Gi-independent increase in cAMP levels.

Authors:  Subhashini Srinivasan; Fozia Mir; Jin-Sheng Huang; Fadi T Khasawneh; Stephen C-T Lam; Guy C Le Breton
Journal:  J Biol Chem       Date:  2009-04-03       Impact factor: 5.157

Review 8.  Antiplatelet drugs: clinical pharmacology and therapeutic use.

Authors:  A S Gallus
Journal:  Drugs       Date:  1979-12       Impact factor: 9.546

9.  The influence of prostaglandin G2 on platelet ultrastructure and platelet secretion.

Authors:  J M Gerrard; D Townsend; S Stoddard; C J Witkop; J G White
Journal:  Am J Pathol       Date:  1977-01       Impact factor: 4.307

10.  A possible role of arachidonic acid in human neutrophil aggregation and degranulation.

Authors:  J T O'Flaherty; H J Showell; P A Ward; E L Becker
Journal:  Am J Pathol       Date:  1979-09       Impact factor: 4.307

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