Cell-free and erythrocytic S-nitrosohemoglobin inhibits human platelet aggregation.

Journal Article

BACKGROUND: Nitric oxide (NO) and related molecules are thought to inhibit human platelet aggregation by raising levels of cGMP. METHODS AND RESULTS: Both oxidative stress (reactive oxygen species) and hemoglobin (Hb) seem to oppose NO effects. A major fraction of NO in the blood is bound to thiols of Hb, forming S-nitrosohemoglobin (SNO-Hb), which releases the NO group on deoxygenation in the microcirculation. Here we show that (1) both cell-free and intraerythrocytic SNO-Hb (SNO-RBC) inhibit platelet aggregation, (2) the oxidation state of the hemes in Hb influences the response--SNO-metHb (which is functionally similar to SNO-deoxyHb) has greater platelet inhibitory effects than SNO-oxyHb, and (3) the mechanism of platelet inhibition by SNO-Hb is cGMP independent. CONCLUSIONS: We suggest that the RBC has evolved a means to counteract platelet activation in small vessels and the proaggregatory effects of oxidative stress by forming SNO-Hb.

Full Text

Duke Authors

Cited Authors

  • Pawloski, JR; Swaminathan, RV; Stamler, JS

Published Date

  • January 27, 1998

Published In

Volume / Issue

  • 97 / 3

Start / End Page

  • 263 - 267

PubMed ID

  • 9462528

International Standard Serial Number (ISSN)

  • 0009-7322

Language

  • eng

Conference Location

  • United States