Hydrogen sulfide inhibits human platelet aggregation

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

doi:10.1016/j.ejphar.2006.12.011

Hydrogen sulfide inhibits human platelet aggregation

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

Fondazione Don Carlo Gnocchi Onlus

Research output: Contribution to journal › Article › peer-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 language	English
Pages (from-to)	65-68
Number of pages	4
Journal	European Journal of Pharmacology
Volume	559
Issue number	1
DOIs	https://doi.org/10.1016/j.ejphar.2006.12.011
Publication status	Published - 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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title = "Hydrogen sulfide inhibits human platelet aggregation",

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.",

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AU - Zagli, Giovanni

AU - Patacchini, Riccardo

AU - Trevisani, Marcello

AU - Abbate, Rosanna

AU - Cinotti, Sandro

AU - Gensini, Gian Franco

AU - Masotti, Giulio

AU - Geppetti, Pierangelo

PY - 2007/3/15

Y1 - 2007/3/15

N2 - 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.

AB - 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.

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KW - Hydrogen sulfide

KW - Platelet inhibition

KW - Thromboembolic disease

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