Hydrogen sulfide inhibits human platelet aggregation

Giovanni Zagli, Riccardo Patacchini, Marcello Trevisani, Rosanna Abbate, Sandro Cinotti, Gian Franco Gensini, Giulio Masotti, Pierangelo Geppetti

Research output: Contribution to journalArticlepeer-review

Abstract

Gaseous mediators such as nitric oxide (NO) play a major regulatory role in the cardiovascular system homeostasis, including platelet aggregation. Here, we investigated whether hydrogen sulfide (H2S), a newly recognized endogenous mediator, can affects aggregation of human platelets, using sodium hydrogen sulfide (NaHS) as H2S-donor. NaHS inhibited platelet aggregation induced by ADP, collagen, epinephrine, arachidonic acid, thromboxane mimetic, U46619, and thrombin. H2S effect was not dependent by cAMP/cGMP generation, NO production or potassium-channels opening. NaHS concentrations (up to 10 mM) did not exert toxic effects on platelet viability. The possible protective role of endogenous H2S in cardiovascular system is discussed.

Original languageEnglish
Pages (from-to)65-68
Number of pages4
JournalEuropean Journal of Pharmacology
Volume559
Issue number1
DOIs
Publication statusPublished - Mar 15 2007

Keywords

  • Cardiovascular risk factor
  • HS
  • Hydrogen sulfide
  • Platelet inhibition
  • Thromboembolic disease

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

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