Hydrogen sulfide inhibits human platelet aggregation.
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 (H(2)S), a newly recognized endogenous mediator, can affects aggregation of human platelets, using sodium hydrogen sulfide (NaHS) as H(2)S-donor. NaHS inhibited platelet aggregation induced by ADP, collagen, epinephrine, arachidonic acid, thromboxane mimetic, U46619, and thrombin. H(2)S 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 H(2)S in cardiovascular system is discussed.
Zagli
Giovanni
G
Department of Critical Care Medicine and Surgery, University of Florence, Florence, Italy. giovanni.zagli@unifi.it
Patacchini
Riccardo
R
Trevisani
Marcello
M
Abbate
Rosanna
R
Cinotti
Sandro
S
Gensini
Gian Franco
GF
Masotti
Giulio
G
Geppetti
Pierangelo
P
D000328:Adult; D001792:Blood Platelets / Q000187:drug effects*; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000502:physiology; D006152:Cyclic GMP / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D006801:Humans; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D066298:In Vitro Techniques; D009569:Nitric Oxide / Q000096:biosynthesis; D010975:Platelet Aggregation Inhibitors; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology
D010975:Platelet Aggregation Inhibitors; D015221:Potassium Channels; D005576:Colforsin; D009569:Nitric Oxide; D000242:Cyclic AMP; D006152:Cyclic GMP; D006862:Hydrogen Sulfide