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Related Experiment Videos

Na+/H+ exchange in PAF-stimulated platelets.

M L Borin1, V G Pinelis, O A Azizova

  • 1Institute of Physico-Chemical Medicine, RSFSR Ministry of Health, Moscow, U.S.S.R.

Journal of Lipid Mediators
|September 1, 1989
PubMed
Summary

Inhibition of sodium-hydrogen exchange (Na+/H+) in human platelets reduces platelet aggregation and calcium signals. This process is crucial for platelet activation, with initial calcium increases essential for Na+/H+ exchange activation.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Physiology

Background:

  • Platelet activation involves complex signaling pathways, including changes in intracellular pH (pHi) and calcium levels.
  • Sodium-hydrogen exchange (Na+/H+) plays a role in regulating pHi, which can influence cellular functions.
  • Platelet-activating factor (PAF) is a potent activator of platelets, but the precise mechanisms linking it to pHi and calcium dynamics are not fully elucidated.

Purpose of the Study:

  • To investigate the role of Na+/H+ exchange in PAF-induced human platelet activation.
  • To determine the relationship between Na+/H+ exchange, pHi changes, and intracellular calcium ([Ca2+]i) mobilization.
  • To explore the signaling pathways involved in PAF-induced Na+/H+ exchange activation, including protein kinase C (PKC).

Main Methods:

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  • Human platelets were loaded with pH-sensitive fluorescent probes (BCECF) and calcium indicators (quin-2).
  • Na+/H+ exchange was inhibited using various methods: substitution of external Na+, decreased extracellular pH, and the specific inhibitor EIPA.
  • Platelet aggregation, pHi changes, and [Ca2+]i were measured following stimulation with PAF or thrombin.
  • The effects of inhibitors of adenylate cyclase, cyclooxygenase, calmodulin-dependent enzymes, and PKC were assessed.

Main Results:

  • Inhibition of Na+/H+ exchange significantly reduced PAF-induced platelet aggregation and the associated increase in [Ca2+]i.
  • PAF stimulation induced biphasic pHi changes, including a sustained alkalinization dependent on Na+/H+ exchange.
  • While PKC activation was involved in tetradecanoyl phorbol acetate (TPA)-induced pHi changes, it was not solely responsible for PAF-induced Na+/H+ exchange.
  • PAF-induced alkalinization required extracellular Ca2+ and an increase in [Ca2+]i, and Na+/H+ exchange potentiated Ca2+ influx.

Conclusions:

  • Na+/H+ exchange is a critical component of PAF-induced human platelet activation, influencing both aggregation and calcium signaling.
  • The activation of Na+/H+ exchange by PAF is dependent on an initial rise in intracellular calcium.
  • Activated Na+/H+ antiport is essential for amplifying calcium influx into platelets, leading to full activation.