Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Immune Environment in Glioblastoma (Feb 2023)
    • Korsmeyer Award 25th Anniversary Collection (Jan 2023)
    • Aging (Jul 2022)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Research letters
    • Letters to the editor
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Research letters
  • Letters to the editor
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Abstract
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Research Article Free access | 10.1172/JCI115540

Molecular and cellular actions of platelet-activating factor in rat heart cells.

C V Massey, T A Kohout, S T Gaa, W J Lederer, and T B Rogers

Department of Medicine, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Massey, C. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Kohout, T. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Gaa, S. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Lederer, W. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Rogers, T. in: JCI | PubMed | Google Scholar

Published December 1, 1991 - More info

Published in Volume 88, Issue 6 on December 1, 1991
J Clin Invest. 1991;88(6):2106–2116. https://doi.org/10.1172/JCI115540.
© 1991 The American Society for Clinical Investigation
Published December 1, 1991 - Version history
View PDF
Abstract

Platelet-activating factor (PAF) is a phospholipid with cardiovascular actions at low concentrations (1-100 nM) but with uncertain direct myocardial actions. We investigated the cellular and molecular effects of PAF on heart cells using isolated adult and neonatal rat myocytes. Addition of PAF, in the superfusion solution, decreased twitch amplitude and contractile velocity in both systems. Concentrations of PAF below 1 nM stimulated reproducible responses with maximal effects seen at 100 nM. These functional actions of PAF could be blocked by the known PAF antagonist, BN 50739, in a dose-dependent manner. Parallel biochemical studies showed that nanomolar PAF rapidly stimulated the phosphoinositide pathway in cultured myocytes, evidenced by the accumulation of [3H]inositol phosphates in prelabeled cultured myocytes. The potency and specificity of PAF, as well as the time course, for the response were nearly identical in the biochemical and functional assays. PAF produced no functional changes in protein kinase C-depleted myocytes, but it did stimulate inositol trisphosphate accumulation in such cells. We conclude that: (a) PAF exerts a direct negative inotropic effect on myocardial tissue; (b) the effects of PAF are mediated by a specific, high affinity cardiac receptor; (c) an underlying biochemical mechanism for the action of PAF includes the activation of the phospholipase C/phosphatidylinositol intracellular signaling pathway, which leads to activation of protein kinase C.

Browse pages

Click on an image below to see the page. View PDF of the complete article

icon of scanned page 2106
page 2106
icon of scanned page 2107
page 2107
icon of scanned page 2108
page 2108
icon of scanned page 2109
page 2109
icon of scanned page 2110
page 2110
icon of scanned page 2111
page 2111
icon of scanned page 2112
page 2112
icon of scanned page 2113
page 2113
icon of scanned page 2114
page 2114
icon of scanned page 2115
page 2115
icon of scanned page 2116
page 2116
Version history
  • Version 1 (December 1, 1991): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Abstract
  • Version history
Advertisement
Advertisement

Copyright © 2023 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts