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Adrenoceptor α2A signalling countervails the taming effects of synchronous cyclic nucleotide-elevation on

Knut Fälker1, Liza U Ljungberg1, Caroline Kardeby1

  • 1Cardiovascular Research Centre (CVRC), School of Medical Sciences, Örebro University, 70182 Örebro, Sweden.

Cellular Signalling
|March 31, 2019
PubMed

Insights

Elevating cyclic GMP (cGMP) and cyclic AMP (cAMP) inhibits platelet activation. Epinephrine, however, restores platelet aggregation by affecting calcium and PI3-K signaling pathways.

Area of Science:

  • Biochemistry
  • Physiology
  • Pharmacology

Background:

  • Vascular endothelium releases autacoids that regulate platelet activation via cyclic nucleotides.
  • Increased cyclic GMP (cGMP) and cyclic AMP (cAMP) inhibit platelet calcium mobilization, dense granule secretion, and aggregation.

Purpose of the Study:

  • To investigate the impact of epinephrine on platelet function in the context of stress-related sympathetic nervous activity.
  • To determine the signaling pathways involved in epinephrine-mediated restoration of platelet aggregation.

Main Methods:

  • Measuring intracellular calcium mobilization, dense granule secretion, and integrin αIIaβ3 activation in human platelets.
  • Assessing platelet aggregation in isolated platelets and heparinized whole blood.
  • Investigating the role of calcium and PI3-K signaling pathways.

Main Results:

  • Combined elevation of cGMP and cAMP inhibited thrombin-induced platelet activation, including integrin αIIaβ3 activation.
  • Epinephrine restored platelet aggregation and signaling events, which were dependent on intracellular calcium and PI3-K signaling.
  • Epinephrine reconstituted platelet aggregation in heparinized whole blood.

Conclusions:

  • Epinephrine can counteract the inhibitory effects of elevated cGMP and cAMP on platelet function.
  • The mechanism involves modulation of calcium and PI3-K signaling pathways.
  • Epinephrine's effect on platelet aggregation may be relevant in vivo, particularly during stress-induced thrombotic events.

Keywords:
Cyclic nucleotideEpinephrineHuman plateletsNitric oxideProstacyclinα(2A) adrenoceptor

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