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Effect of platelet-activating factor (PAF) on sodium calcium exchange in cardiac sarcolemmal vesicles

H P Meng1, M J Kutryk, G N Pierce

  • 1Division of Cardiovascular Sciences, St. Boniface General Hospital Research Center, Winnipeg, Canada.

Insights

Platelet-activating factor (PAF) inhibits cardiac Na(+)-Ca2+ exchange, but this effect is not receptor-mediated. This inhibition likely does not contribute to PAF's negative inotropic action on the heart.

Area of Science:

  • Cardiovascular Physiology
  • Cellular Electrophysiology
  • Pharmacology

Background:

  • Platelet-activating factor (PAF) is implicated in cardiac function.
  • Understanding PAF's mechanism of inotropic action requires investigating its effects on ion transport.

Purpose of the Study:

  • To elucidate the mechanism by which PAF affects Na(+)-dependent calcium uptake in myocardial sarcolemmal vesicles.
  • To determine if PAF's action on Na(+)-Ca2+ exchange is receptor-mediated.

Main Methods:

  • Utilized myocardial sarcolemmal vesicles to study Na(+)-dependent calcium uptake.
  • Assessed the effects of varying concentrations of PAF and Lyso-PAF on Na(+)-Ca2+ exchange kinetics.
  • Investigated the role of PAF receptors using the antagonist CV-3988.
  • Measured passive Ca2+ permeability and binding to cardiac sarcolemma.

Main Results:

  • PAF significantly inhibited Na(+)-Ca2+ exchange in a dose-dependent manner.
  • PAF reduced the Vmax of Na(+)-Ca2+ exchange without altering Km.
  • The PAF receptor antagonist CV-3988 did not block PAF's inhibitory effect on Na(+)-Ca2+ exchange.
  • PAF increased passive Ca2+ permeability and binding to cardiac sarcolemma.

Conclusions:

  • PAF inhibits cardiac Na(+)-Ca2+ exchange through a non-receptor-mediated mechanism.
  • The observed inhibition of Na(+)-Ca2+ exchange by PAF is unlikely to be the primary cause of its negative inotropic effect in physiological conditions.

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